Prof Derrik soon Anki Flashcards

Question

How does CNS function to keep consciousness? - [...] - [...]

Answer 1

How does CNS function to keep consciousness? - Reticular activating system of brainstem - Adequate cerebral hemispheric function (in acute interference of hemispheric function, decreased level of consciousness is more likely to occur if left side is involved)

Answer 2

Which substrates and electrolytes are esp impt for maintaining consciousness? - Glucose (and ketones) - Electrolytes (Na, K, Ca)

Answer 3

What is the difference between sleep and impaired consciousness? whether the person can be woken up :/

Answer 4

"What medical terms are used to define the different states of impaired consciousness? 1. Lethargy - difficulty in maintaining awake state 2. Obtundation - responds to non-pain stimuli 3. Stupor - responds to pain 4. Coma - no response ""Mn - Let Out Stupid Comments"" Differentiating sleep and impaired consciousness: Sleeping people can illicit some sort of response."

Answer 5

Evaluation of a person with impaired consciousness: 1. Orientation and Memory (time,space,person,digit span, recall of items after 5 mins) 2. Conscious level 3. Brainstem reflex function 4. Motor and sensory function, and coordination

Answer 6

Glasgow Coma Scale (GCS) is used to assess level of consciousness and it is comprised of 3 parts (E,V,M) 1. Eye-opening response 2. Best verbal response 3. Best motor response Outline some limitations of using the GCS (IMPT!!) - Evaluating eye opening if there is severe orbito-facial injury - Assessment of verbal function if intubated - Inability to score differences between right- and left-sided

Answer 7

Glasgow Coma Scale (GCS) is used to assess level of consciousness and it is comprised of 3 parts (E,V,M) 1. Eye-opening response 2. Best verbal response 3. Best motor response Outline some limitations of using the GCS (IMPT!!) - Evaluating eye opening if there is severe orbito-facial injury - Assessment of verbal function if intubated - Inability to score differences between right- and left-sided

Answer 8

What are the common causes for impairment of consciousness? - Traumatic brain injury - Cerebrovascular event (hemorrhage, thrombosis, embolism, vasculitis) - Seizures or status epilepticus (post-ictal state) - Syncope (transient cerebral hypoperfusion) - CNS Infection (meningitis, encephalitis, brain abscess) - Post-infectious/inflammatory reaction/disorder (ADEM, MS) - Medications (overdose of me

Answer 9

Prolonged impairment of consciousness (comatose state) occurs if large areas of the brain is affected. Injury/insult to the brain persist depending on the cause Name some causes of comatose state - Traumatic brain injury - Cerebrovascular accident (Hemorrhage, Thrombosis, Embolism, Vasculitis) - CNS Infection (viral/autoimmune encephalitis) - Refractory status epilepticus and drugs. think about th

Answer 10

Syncope definition (IMPT!!!) A paroxysmal event with loss of consciousness and postural tone due to cerebral hypoperfusion, with spontaneous recovery. What are the causes of Syncope? - Decreased Cerebral perfusion - Decreased Oxygenation in the blood Syncope usually caused by abrupt reduction/cessation of energy substrates to the cerebral cortex through sudden decrease in well oxygenated blood sup

Answer 11

What are the classical clinical features of syncope? - Loss of consciousness & postural tone (in definition) - Pallor, sweating - Whole episode usually last less than 30 seconds, spontaneous recovery) - Convulsions, a few irregular myoclonic jerks, tonic flexion/extension, complex movements, autmatisms (licking, chewing, fumbling) - Visual and auditory hallucinations - Sudden onset, urinary incont

Answer 12

What are the classical clinical features of syncope? - Loss of consciousness & postural tone (in definition) - Pallor, sweating - Whole episode usually last less than 30 seconds, spontaneous recovery) - Convulsions, a few irregular myoclonic jerks, tonic flexion/extension, complex movements, autmatisms (licking, chewing, fumbling) - Visual and auditory hallucinations - Sudden onset, urinary incont

Answer 13

What are the classical clinical features of syncope? - Loss of consciousness & postural tone (in definition) - Pallor, sweating - Whole episode usually last less than 30 seconds, spontaneous recovery) - Convulsions, a few irregular myoclonic jerks, tonic flexion/extension, complex movements, autmatisms (licking, chewing, fumbling) - Visual and auditory hallucinations - Sudden onset, urinary incont

Answer 14

What are the 2 categories of syncope? - neurally-mediated (neurocardiogenic or reflexmediated) - cardiogenic (cardiac rhythm or structural cardiacdisorders) Read below

Answer 15

Definition of seizure Sudden and unusual / erratic electrical changes in the cortical neurons that we cannot control. Causes brief alteration in a person’s consciousness, sensation, movements or actions Like derek said, seizures are basically power surges.

Answer 16

Causes of seizure? acute systemic metabolic disturbance/disturbance of brain structure or metabolism, causing irritation of the cortex - Hypoglycemia or electrolyte disturbance - Head trauma - Stroke - Alcohol & alcohol withdrawal - Drugs & drug withdrawal The label “epilepsy” is not used because the seizures are closely related to the underlying temporary disturbance of brain function Seizures ar

Answer 17

What is epilepsy? A chronic condition characterized by a predisposition to recurrent, usually spontaneous (not reflex) seizures multiple seizures (not in same day) = epilepsy

Answer 18

"""Fit vs Faint"" How to diagnose? (IMPT!!!) - Clinical history is key. Based on detailed description of events experienced by the patient and/or eye-witness before, during and after a event/seizure (blow by blow) - Video-recording of event/Home recording (gold standard lol) - (if not) Witness should attend consultation/be telephoned - (if not) Written account ""HH ah, how to diagnose Fit vs Faint

Answer 19

"Name 2 differential diagnosis of epilepsy? - Breath Holding Spell (cyanotic) - Breath Holding Spell (pallid) What? I don't understand this slide.. ""Breath-holding spells are brief periods when young children stop breathing for up to 1 minute. These spells often cause a child to pass out (lose consciousness). Breath-holding spells usually occur when a young child is angry, frustrated, in pain, or

Answer 20

what are signs of epileptic seizures? - Sudden stiffening followed by repetitive shakes or jerks - Auras, coloured orbs, automatisms, psychic auras, terror - Pre-ictal cry - Disrupted breathing - Incontinence - Prolonged duration - Prolonged disorientation after event with sleepiness and aching Just follow Derek's.

Answer 21

in neuro nomenclature, Myelo- refers to spinal cord but can also refer to myeloid lineages eg myelosuppression. Radiculo - refers to roots

Answer 22

Examples of disease at levels of nerves. Mononeuropathy, Mononeuritis multiplex, Peripheral neuropathy Roots --> Plexus --> Nerve --> NMJ --> Muscle Roots, Plexus, Nerves considered LMN NMJ, muscles considered neuromuscular complex Peripheral neuropathies can affect neurons of any length, but normally target neurons of a specific length.

Answer 23

NMJ and Muscle lesions What are signs of proximal myopathy (muscle lesions)? - Proximal weakness - Wasting without fasciculations - +/- Pseudohypertrophy What are signs of NMJ lesions? - Proximal weakness - Ocular weakness (think myasthenia gravis) - Fatiguability (think myasthenia gravis) Why does NMJ and muscle lesions both present with proximal weakness? Why not distal? Proximal muscles exert m

Answer 24

Duchenne muscular dystrophy (DMD) is a X-linked genetic disorder characterized by progressive muscle degeneration and weakness. Which gene is mutated in DMD? Dystrophin gene on X chromosome. Dystrophin is a component of the membrane cytoskeleton in normal muscle, contributes to membrane stability. What does DMD patients present with? - Proximal weakness - Affect heart and respiratory muscles (deat

Answer 25

What in the world is myasthenia gravis? weakness and increasing fatigue after repetitive use of any of the muscles under your voluntary control Cause? Ab mediated autoimmune reaction!! AchRAbs (Acetylcholine Receptor AntiBodies) that competes with Ach for AchRs. Why increasing fatique with repetitive muscle use? At first got more Ach than AchRAb. But with sustained contraction, the exhaustion of A

Answer 26

General observations about LMN (roots, plexus and nerve) Are part of LMN, so will have areflexia, hypotonia, wasting, fasciculations, weakness, sensory abnormalities General observation about nerves Long nerves more vulnerable to systemic insults than short nerves. Henceit affects the extremities of limbs first (glove and stocking distribution weakness and numbness) (all 4 limbs, but usually feet

Answer 27

median nerve kena whack = Carpel Tunnel Syndrome Radial nerve kena whack = Saturday Night Palsy Ulnar nerve kena whack = Cubital tunnel syndrome Just read the slides.

Answer 28

Can someone with saturday night palsy extend his elbows? Yes! because damage comes AFTER nerve to triceps

Answer 29

Signs of damage to sciatic nerve: 1. Foot drop (weak dorsiflexion) 2. Weak plantarflexion 3. Weak hip adduction More often the common peroneal/ fibular nerve is squished 1. Foot drop (weak dorsiflexion) 2. Strong plantarflexion (tibial nerve intact) 3. Strong hip adduction 4. Strong inversion (tibialis posterior- tibial n) Sciatic does hip adduction Sciatic splits into common peroneal and tibial n

Answer 30

Lumbosacral plexus injury tends to be at level of L4-S1 Can mimic sciatic nerve injuries (same roots) Eh slides say this is impt eh:

Answer 31

"right cerebellum lesion presentation ""mn - DDDANISH"" Dysdiadochokinesia - Inability to perform rapid alternating movements Dysmetria - inability to judge distance Dyssynergy - loss of coordination of motor movement Ataxia - incoordination of movements Nysagmus - eyes make repetitive, uncontrolled movements Intention tremor - movement tremors Scanning speech/stacatto - ataxic dysarthria in which

Answer 32

Weakness to whole body down the neck. Which level of damage? Cervical C5

Answer 33

There are a heck load of nociceptors in our head. examples of where they can they be found? scalp bone (esp periosteum) blood vessels mucosal linings meninges cranial nerves ears eyes teeth Does the parenchyma hurt? NO!!!! Because there are no nociceptors there. That's why neurosurgery is done while conscious Strokes could hurt due to: Process: Dissections or bleeds Consequence: Raised-ICP Special

Answer 34

What are the 2 most important Red flags of sinister headaches? (IMPT!!!) - Raised ICP - Neurological deficit Other redflags? (but not seen in all sinister headaches) - tempo (sudden onset or evolving) - constitutional (weight loss/ fever/ confusion and seizures) - elderly (think tumours and temporal arteritis) - meningitic features (fever, headache, photophobia, neck ache etc) In the elderly tempo

Answer 35

Features of raised ICP? What makes it worse? (IMPT!!!!) - Clear postural/pressure features (worse on cough/sneezing/bending over/visual obscurations on bending over) - Worse in night than day - Wake up with headache + vomitting - Pulsatile tinnitus Pt 1, anything that strains the body would cause pain. Visual obstructions when bending over is a serious sign because it means that ICP is high enough

Answer 36

What is the diff between raised ICP and glaucoma? Raised ICP impedes venous flow from back of eye --> optic disc swelling and oedema (blurred margins), which is collectively called papilloedema Glaucoma pressure is inside the eye --> no disc swelling, only enhanced disc cupping which 3 cranial nerves are vulnerable to raised ICP? Why? CN VI (most vulnerable) as it emerges from the lip of foramen m

Answer 37

"Other features of sinister headaches A thunderclap headache, also referred to as a lone acute severe headache, is a headache that is severe and sudden-onset. Which causes of thunderclap headaches are sinister and must be excluded? (""VSD"") (IMPT!!!!) - Subarachnoid haemorrhage!!!! - Venous sinus thrombus - Dissection Which causes of thunderclap headaches are non-sinister (primary headaches) and Migraine, cluster

Answer 38

When we do lumbar puncture to check for bleeding in CSF, how do we know if it's not bleeding from the needle injury? Instead of immediately, wait for 8 hours. look for breakdown of blood products (bilirubin - xanthochromia) We dont look for RBCs cuz if the infiltrating needle passes through a vessel before the CSF (traumatic tap), then we'll get a false positive result from the test. 8/24 is also

Answer 39

What causes of headaches with neck stiffness are sinister? Meningism! So either infective meningitis (irritation from bacteria) or SAH (irritation from blood) What causes of headaches with neck stiffness are NOT sinister? Cervicogenic headache (tight neck muscles) Neck stiffness is a sign of meningitis because? you stretch meninges when you bend your neck.

Answer 40

"Temporal tenderness/Jaw claudication (headache pain on chewing) is a sign of temporal arteritis, a sinister headache Why is it important to diagnose immediately? If missed, causes bilateral blindness in 50% of untreated patients!!! Definitive test for temporal arteritis? Temporal artery biopsy (but beware of skip lesions) If headache in elderly patient, suspect temporal arteritis and just prescribe High dose steroids (temporal arteritis is a form of vasculitis). This is a sinister headache.

Answer 41

True or False? 1. CT scans can diagnose meningitis Untrue; The best diagnostical method is a lumbar puncture with CSF examination 2. CT scans can predict those who will cone Untrue 3. A normal CT scan means safe to do LP Whether or not a patient presents with edema on CT scan does not affect the safety of an LP 4. Lumbar puncture causes coning Untrue, no evidence to say so For pt 4. it's not entir

Answer 42

"List the conditions that are confined to CNS (IMPT!!!) - Stroke - Epilepsy - Multiple sclerosis - Dementias - Parkinson Disease - Encephalitis - Meningitis (can affect anywhere with meninges) List the conditions that are confined to PNS (IMPT!!!) - Brachial neuritis - Peripheral neuropathies inc GBS (Guillain Barre) - Mononeuritis Multiplex - Myasthenia Gravis - Myositis List the conditions that

Answer 43

"List the conditions that are confined to CNS (IMPT!!!) - Stroke - Epilepsy - Multiple sclerosis - Dementias - Parkinson Disease - Encephalitis - Meningitis (can affect anywhere with meninges) List the conditions that are confined to PNS (IMPT!!!) - Brachial neuritis - Peripheral neuropathies inc GBS (Guillain Barre) - Mononeuritis Multiplex - Myasthenia Gravis - Myositis List the conditions that

Answer 44

What presentations would suggest CNS lesion? (vvvvv IMPT!!!) - UMN lesions - Cerebellar/ Basal gangia (nuclei symptoms) eg ataxia - Cognitive signs - Visual field defects (all visual field defects are CNS problems eg hemianopia) What presentations would suggest PNS lesion? (vvvvv IMPT!!!) - Exclusively LMN issues - Muscle/ NMJ issues (eg Myasthenia Gravis, peripheral neuropathies) LMN mostly PNS e

Answer 45

What presentations would suggest CNS lesion? (vvvvv IMPT!!!) - UMN lesions - Cerebellar/ Basal gangia (nuclei symptoms) eg ataxia - Cognitive signs - Visual field defects (all visual field defects are CNS problems eg hemianopia) What presentations would suggest PNS lesion? (vvvvv IMPT!!!) - Exclusively LMN issues - Muscle/ NMJ issues (eg Myasthenia Gravis, peripheral neuropathies) LMN mostly PNS e

Answer 46

What is a reflex arc made of? Afferent limb (sensory neuron) + efferent limb (LMN) What are the physiological functions of the reflex arc? - Prevents overstretching of muscle - protective - Helps maintain posture - Generates tone UMN input modulates and regulates reflex.

Answer 47

What is a reflex arc made of? Afferent limb (sensory neuron) + efferent limb (LMN) What are the physiological functions of the reflex arc? - Prevents overstretching of muscle - protective - Helps maintain posture - Generates tone UMN input modulates and regulates reflex.

Answer 48

Movement has several elements: - Power - Coordination - Quantity

Answer 49

Do motor neurons pass through the cerebellum? No Therefore in cerebellar dysfunction there would be pure ataxia and cerebellar signs. Other signs would include: Arms: Rebound, Finger nose dysmetria, Dysdiadochokinesis Legs: Heel shin Ataxia, Broad Based Gait Eyes: Nystagmus, Dysmetric Saccades, Broken Pursuit Mouth: Cerebellar dysarthria Trunk: Truncal Ataxia Dysmetria - terminal tremors Basically

Answer 50

Which CN nuclei are in: Midbrain: III, IV Pons: V, VI, VII, VIII Medulla: IX, X, XII CN that arise from the midpontine level would be CN VI, VII and VIII. The only CN that arises from the pons proper would CN V. CN nuclei lesons are always LMN lesions (NOT UMN!!). Motor cranial nerves are analogous to LMN. 2 (CN 1 & 2), 2, 4, 3, 1 (CN 11)

Answer 51

"Subcortical lesions (white matter) tend to give rise to pure motor or sensory syndromes. Cortical lesions (grey matter) tend to give rise to motor and/ or sensory syndromes PLUS cortical features. Deficits would include: Language: Dysphasia Spelling: Dysgraphia Arithmetic: Dyscalculia Visuospatial orientation: Agnosias Awareness: Neglect Epilepsy starts in the cortex, and can begin with 1 neuron.

Answer 52

Do motor neurons pass through the cerebellum? No Therefore in cerebellar dysfunction there would be pure ataxia and cerebellar signs. Other signs would include: Arms: Rebound, Finger nose dysmetria, Dysdiadochokinesis Legs: Heel shin Ataxia, Broad Based Gait Eyes: Nystagmus, Dysmetric Saccades, Broken Pursuit Mouth: Cerebellar dysarthria Trunk: Truncal Ataxia Dysmetria - terminal tremors Basically

Answer 53

Summary of lesions (IMPT!!!) Brain: Cerebrum: UMN, Contralateral Brainstem: UMN, Contralateral (+/- ipsilateral face because of CN VII double innervation) Cerebellum: Pure ataxia, Ipsilateral Cord: Cervical: UMN, sphincteric involvement, sensory level, LMN Thoracic: UMN, sphincteric involvement, sensory level, LMN LS: UMN, sphincteric involvement, sensory level, LMN

Answer 54

Summary of lesions (IMPT!!!) Brain: Cerebrum: UMN, Contralateral Brainstem: UMN, Contralateral (+/- ipsilateral face because of CN VII double innervation) Cerebellum: Pure ataxia, Ipsilateral Cord: Cervical: UMN, sphincteric involvement, sensory level, LMN Thoracic: UMN, sphincteric involvement, sensory level, LMN LS: UMN, sphincteric involvement, sensory level, LMN

Answer 55

Anterior cord syndrome affects the spinothalamic +/- lateral tracts Posteior cord syndrome affects the DCML and corticospinal tracts Brown-Sequard Syndrome affects the ALL 3 tracts.

Answer 56

Why are reflexes still present in muscle or NMJ lesions? Lesions here tend to be partial and cause partial weakness. Therefore there will still be a reflex until the weakness is super profound. While a lesion in LMN is at a neuron so lesion tends to be complete --> areflexia So in diseases such as polymyositis and Guillain-Barre, reflexes would still remain. Repeat card. IMPT!

Answer 57

Common radiculopathies: - C5-7 - L4-S1 General presentations: Sensory and motor distributions confined to single nerve roots

Answer 58

Summary of presentations of PNS lesions. Think root, plexus, nerve, NMJ, Muscle. Then think pattern, distribution and comments.

Answer 59

Common injuries of the plexi: Brachial: 75% of the brachial plexus injuries occur at the roots/ trunks. In anatomical terms it would mean that they occur above the clavicle. The parts below are well protected. Erb's palsy level? (C5-C6) Features? Shoulder rotated forward Affected arm diminished in length and girth Muscle atrophy of the affected arm Waiter's tip deformity of the affected wrist Cerv

Answer 60

Common injuries of the plexi: Brachial: 75% of the brachial plexus injuries occur at the roots/ trunks. In anatomical terms it would mean that they occur above the clavicle. The parts below are well protected. Erb's palsy level? (C5-C6) Features? Shoulder rotated forward Affected arm diminished in length and girth Muscle atrophy of the affected arm Waiter's tip deformity of the affected wrist Cerv

Answer 61

Common injuries of the plexi: Brachial: 75% of the brachial plexus injuries occur at the roots/ trunks. In anatomical terms it would mean that they occur above the clavicle. The parts below are well protected. Erb's palsy level? (C5-C6) Features? Shoulder rotated forward Affected arm diminished in length and girth Muscle atrophy of the affected arm Waiter's tip deformity of the affected wrist Cerv

Answer 62

Approaching seizures: Just read below

Answer 63

There are a heck load of nociceptors in our head. examples of where they can they be found? scalp bone (esp periosteum) blood vessels mucosal linings meninges cranial nerves ears eyes teeth Does the parenchyma hurt? NO!!!! Because there are no nociceptors there. That's why neurosurgery is done while conscious Strokes could hurt due to: Process: Dissections or bleeds Consequence: Raised-ICP Special

Answer 64

What are the 2 most important Red flags of sinister headaches? (IMPT!!!) - Raised ICP - Neurological deficit Other redflags? (but not seen in all sinister headaches) - tempo (sudden onset or evolving) - constitutional (weight loss/ fever/ confusion and seizures) - elderly (think tumours and temporal arteritis) - meningitic features (fever, headache, photophobia, neck ache etc) In the elderly tempo

Answer 65

Revision: raised ICP occurs when: Excess in the skull: Malignant/Idiopathic intracranial HTN Extra stuff that's not meant to be there: Tumours, absesses, brain swelling Blockage of drainage systems: - Venous (sinus) thrombosis - Obstructive/ non-communicating Hydrocephalus

Answer 66

Normal vs raised-ICP fundus: Normal: - Crisp margins - Normal vasculature Raised-ICP: - Blurred margins --> papilloedema - Disrupted vasculature, microhaemorrhages Think margin and vasculature!! Blurred margins due to disc swelling and oedema from obstruction of venous drainage from back of eye

Answer 67

Management of haemorrhagic bleeds in the brain? - Manage BP - Monitor glucose levels - Ventilate if required - Ensure that temperature is fine BP, blood sugar, ventilation, temperature. Basic parameters.

Answer 68

What are clinical features of venous sinus thrombosis? - Headache +/- focal signs - Seizures - Raised ICP (cuz its sinister) Venous sinus thrombosis occurs in patients with? - Coagulation disorders and dehydration ((pregnant women are susceptible) - Post COVID How to investigate? How to treat? Investigate with venography (CT or MR), treat via anti-coagulation What sign is elicited in venous sinus

Answer 69

What are clinical features of venous sinus thrombosis? - Headache +/- focal signs - Seizures - Raised ICP (cuz its sinister) Venous sinus thrombosis occurs in patients with? - Coagulation disorders and dehydration ((pregnant women are susceptible) - Post COVID How to investigate? How to treat? Investigate with venography (CT or MR), treat via anti-coagulation What sign is elicited in venous sinus

Answer 70

Why are photophobia and phonophobia not considered sinister symptoms? They're both present in common migraine headaches.

Answer 71

Carotid artery dissection features? - Tearing neck pain (classic, cannot forget) - Neurological deficit (Stroke, CN XII palsy, Horner's) - +/- history of head manipulation (dont anyhow go for neck massage) Carotid artery dissection - Anticoagulation - Angioplasty - not entirely proven yet General concept (very deep concepts, need to refine!!) Anticoagulation for conditions that predispose to clott

Answer 72

Meningism is a clinical syndrome denoting irritation of the meninges. Meningism is said to be a triad of: - Headache - Neck stiffness - Photophobia (not always) What are the 2 signs that can be elicited from meningitis? Kernig's and Brudzinski's Fever might not be part of the triad, in case meningism isn't caused by an actual infection.

Answer 73

Possible causes and effects of CNS infection: Abscess: Rare, normally in immune compromised Clinically: Fever, headache, focal neurology Meningitis: Bacterial- Meningococcus, Pneumococus Viral Clinically: Fever, Meningism, Altered sensorium Encephalitis: Tends to be viral (HSV) Or bacterial spread from meninges (in that case would be meningo-encephalitis) Clinically: Altered sensorium, seizures, f

Answer 74

Possible causes and effects of CNS infection: Abscess: Rare, normally in immune compromised Clinically: Fever, headache, focal neurology Meningitis: Bacterial- Meningococcus, Pneumococus Viral Clinically: Fever, Meningism, Altered sensorium Encephalitis: Tends to be viral (HSV) Or bacterial spread from meninges (in that case would be meningo-encephalitis) Clinically: Altered sensorium, seizures, f

Answer 75

We suspect meningitis when the patient has: - Fever and meningism (headache, neckstiffness +/- photophobia) - May or may not be confused What are the complications of meningitis? - Neurological deficit, CN deficit, Seizures - Brain infarction - Meningeal fibrosis and hydrocephalus - Raised ICP - Mental retardation (children) What does meningitis with rashes points towards? Neisseria meningitidis!!

Answer 76

Now what about brain tumours? How do they present classically? - Raised ICP headache which has been evolving for months (not acute/sudden. If acute then likely SAH) - Neurological deficit - Associated constitutional features (weight loss which is classical of cancer) - Seizures Therefore, every patient who presents with a headache needs a full neurological examination (huh wtf seriously??? No need

Answer 77

Summary of the lecture: Uncle with tender head refers to temporal arteritis.

Answer 78

What is the most common cause of acute stroke? (IMPT!!!) Ischaemic stroke (85%), normally seen in older patients (atherosclerosis, HTN etc) Which is the most dangerous type of stroke? SAH (always this guy) (25% die before reach ED), normally seen in younger patients (berry aneurysms/arteriovenous malformations) Are parenchymal strokes more serious or SAH? SAH What are the signs of acute stroke? -

Answer 79

What is the most common cause of acute stroke? (IMPT!!!) Ischaemic stroke (85%), normally seen in older patients (atherosclerosis, HTN etc) Which is the most dangerous type of stroke? SAH (always this guy) (25% die before reach ED), normally seen in younger patients (berry aneurysms/arteriovenous malformations) Are parenchymal strokes more serious or SAH? SAH What are the signs of acute stroke? -

Answer 80

What are the main supplies of blood to the brain? 1. Carotid arteries (80%) 2. Vertebral arteries (20%) What does these arteries interconnect to form? What is its significance? Circle of Willis at base of brain. Provides collateral bloodflow. Which vessel from the Circle of Willis contributes the most to cerebral circulation? MCA!! So most strokes have to do with MCA

Answer 81

How do we gauge severity of stroke? 1. GCS (max score 15, get worried at 13)(limited use in stroke. Dont use) 2. NIHSS (max score 42, >10 would suggest 80% chance of severe damage or death in hospital Recall that GCS max score is 15, min score is 3 and below 13 is worrying. NIHSS = National Institutes of Health Stroke Scale When using the NIHSS you must remember to take 2 measurements; one when th

Answer 82

Outline the risk factor for strokes. Which one is the strongest modifiable risk factor? (vvvvvvv IMPT!!!) 1. HTN (strongest modifiable risk factor for all strokes) 2. DM 3. High lipids 4. Smoking 5. AF rather standard answers but need to know because these are what we target in secondary prevention Just reducing BP by 9mmHg can reduce stroke risk by 44%!! Treatment for stroke from DM is harder tha

Answer 83

FAST assessment for strokes? (IMPT!!!) 1. Facial droop (weakness/numbness) 2. Arm drift (balance, coordination) 3. Slurred speech (language) 4. Time (CALL FOR HALP!! 995.) What is used for post stroke functional assessment? What does it measure? Modified Rankin Score (MRS), used to measure dependance 1 min of stroke kills 1.9 neurons in the brain

Answer 84

Why are stroke units important? improves outcomes!! Not a trivial card.

Answer 85

Acute stroke patient management? 1. Blood pressure 2. BGL 3. Body temperature 4. Neurological observation It's about the same as seizure management. Body temperature, BP and glucose are all parts of this. Can add respiratory support etc for either. General medical measures include - hydration - feeding - positioning - rehab TLDR to manage stroke - IV tPA - Urgent imaging to exclude bleeding - Cont

Answer 86

Should we treat HTN in patients with early ischemic stroke? No, unless hypertensive encephalopathy, myocardial ischemia, CHF, aortic dissection. Mild and moderately elevated BP not routinely lowered!! Reasons for not treating HTN? 1. Blood pressure returns to baseline in a few days 2. BP lowering can cause infarct extension because of presence of an ischaemic penumbra and loss of autoregulation Re

Answer 87

Should we treat HTN in patients with early ischemic stroke? No, unless hypertensive encephalopathy, myocardial ischemia, CHF, aortic dissection. Mild and moderately elevated BP not routinely lowered!! Reasons for not treating HTN? 1. Blood pressure returns to baseline in a few days 2. BP lowering can cause infarct extension because of presence of an ischaemic penumbra and loss of autoregulation Re

Answer 88

First line drug for stroke? IV t-PA (thrombolytic, only 1 med lol!! time to specialize in stroke??) Why should reasonable glycemic control be maintained in all acute stroke patients.? Hyperglycaemia associated with worse outcomes and increased risk of ICH in patients treated with t-PA (fibrinolytic) Why should measure be taken to combat fever in acute stroke patients? Fever is associated with wors

Answer 89

First line drug for stroke? IV t-PA (thrombolytic, only 1 med lol!! time to specialize in stroke??) Why should reasonable glycemic control be maintained in all acute stroke patients.? Hyperglycaemia associated with worse outcomes and increased risk of ICH in patients treated with t-PA (fibrinolytic) Why should measure be taken to combat fever in acute stroke patients? Fever is associated with wors

Answer 90

When we use IV t-PA, what are we trying to save? The ischaemic penumbra, which is an area of reduced perfusion (<40% blood flow). Ischaemic core abit 没救 liao Outline the t-PA protocol in stroke. - No anticoagulants and antiplatelets for 24hrs - Maintain BP in recommended range (<180/105mmHg) - Repeat CT in 24hrs and stat if ICH is suspected What are the Inclusion criteria for t-PA treatment? - Pla

Answer 91

When we use IV t-PA, what are we trying to save? The ischaemic penumbra, which is an area of reduced perfusion (<40% blood flow). Ischaemic core abit 没救 liao Outline the t-PA protocol in stroke. - No anticoagulants and antiplatelets for 24hrs - Maintain BP in recommended range (<180/105mmHg) - Repeat CT in 24hrs and stat if ICH is suspected What are the Inclusion criteria for t-PA treatment? - Pla

Answer 92

When we use IV t-PA, what are we trying to save? The ischaemic penumbra, which is an area of reduced perfusion (<40% blood flow). Ischaemic core abit 没救 liao Outline the t-PA protocol in stroke. - No anticoagulants and antiplatelets for 24hrs - Maintain BP in recommended range (<180/105mmHg) - Repeat CT in 24hrs and stat if ICH is suspected What are the Inclusion criteria for t-PA treatment? - Pla

Answer 93

Future of stroke treatment Endovascular treatment of acute ischaemic stroke? - Merci Retriever - Stentrievers Treatment of malignant hemispheric infarction? - Decompressive surgery (release pressure through the skull). Early decompression yields better results TLDR, we spam tPA now but next time maybe can use stentrievers and decompressive surgery.

Answer 94

Read below for cases. In case 1 there is almost 100% recovery in the taxi driver after t-PA treatment.

Answer 95

Imaging: Where are the watershed infarctions in the brain? Cortical Border Zone: ACA MCA Internal Border Zone: LCA MCA Cortical Border Zone MCA PCA Watershed regions basically are tissues between borders of arterial supply, which are furthest away from the artery hence vulnerable to ischemia and infarction. LCA stands for penetrating arteries

Answer 96

"Imaging: Anterior circulation stroke Anterior circulation would involve the MCA and ACA. What are the early signs of acute MCA infarct that can be seen on CT? (IMPT!!!) - Dense MCA sign - Hypodensity in brain tissue - Obscuration of lentiform nucleus (cuz its the earliest area to be affected) - ""Insular ribbon"" sign - Sulcal effacement/mass effect On CT, 60% of acute infarcts are seen within 3-

Answer 97

Imaging: Posterior circulation stroke The posterior circulation would involve the PCA, SCA, AICA or PICA. The names here are a bit more confusing, so refer to this. Right anterior cerebellar artery stroke. Look at the hypodense area in the right cerebellum. Right posterior inferior cerebellar artery. When imaging the brain you can use the axial-coronal-sagittal planes to localise lesions. This is

Answer 98

"Imaging: Other imaging of infarction Refer below. These could involve any or all of the main vessel supplies to the brain. Note the hyperdense area on DWI (left) would (should) overlap/ correspond with the hypodense area on ADC (right). This one is harder to take note of, but clinical Hx would be helpful. Early infarctions/ small infarctions are easier to see on MRI than CT This is where you see

Answer 99

Imaging: Mimickers of stroke What are the conditions that mimics strokes on imaging? - cerebral venous thrombosis (venous sinus thrombosis?) - SDH/EDH/SAH (extra-axial) - Parenchymal bleeds (intra-axial) - Vascular malformations - Tumours Why would these mimic strokes? They can create hypodensities/ hyperdensities on CT/ MRI, therefore you must correlate with clinical Hx. Basically: SAH/EDH/SDH, T

Answer 100

Imaging: Mimickers of stroke What are the conditions that mimics strokes on imaging? - cerebral venous thrombosis (venous sinus thrombosis?) - SDH/EDH/SAH (extra-axial) - Parenchymal bleeds (intra-axial) - Vascular malformations - Tumours Why would these mimic strokes? They can create hypodensities/ hyperdensities on CT/ MRI, therefore you must correlate with clinical Hx. Basically: SAH/EDH/SDH, T

Answer 101

Imaging: What are the routine MRI Brain sequences? DWI with ADC Diffusion-weighted imaging (DWI) Apparent Diffusion Coefficient (ADC)

Answer 102

In basal ganglia lesions, we can have either too much (eg - dyskinesia) or too little (eg - Parkinsonism) movement.

Answer 103

Parkinsonism is a clinical syndrome that is normally associated with? (IMPT!!!!!) 1. Lead pipe rigidity (lack of voluntary movement) 2. Bradykinesia (immobility) 3. Resting tremors What are some causes of Parkinsonism? - Idiopathic Parkinson's disease - Neuroleptic medication (EPSE - typical psychotics etc) - Wilson disease - Infective encephalitis - Vascular Parkinsonism - Parkinson Plus Syndrome

Answer 104

Parkinsonism is a clinical syndrome that is normally associated with? (IMPT!!!!!) 1. Lead pipe rigidity (lack of voluntary movement) 2. Bradykinesia (immobility) 3. Resting tremors What are some causes of Parkinsonism? - Idiopathic Parkinson's disease - Neuroleptic medication (EPSE - typical psychotics etc) - Wilson disease - Infective encephalitis - Vascular Parkinsonism - Parkinson Plus Syndrome

Answer 105

Lead-pipe rigidity is a feature of Parkinsonism. What is rigidity? Rigidity is the resistance to passive movement. How does extrapyramidal rigidity present vs UMN rigidity (hypertonia)? Lead-pipe (hard all the time) vs Clasp knife (easy in some planes of movement) In UMN rigidity (clasp knife), why is it resistance found in only some ranges of motion? - Certain sets of muscles are stronger than an

Answer 106

Lead-pipe rigidity is a feature of Parkinsonism. What is rigidity? Rigidity is the resistance to passive movement. How does extrapyramidal rigidity present vs UMN rigidity (hypertonia)? Lead-pipe (hard all the time) vs Clasp knife (easy in some planes of movement) In UMN rigidity (clasp knife), why is it resistance found in only some ranges of motion? - Certain sets of muscles are stronger than an

Answer 107

Bradykinesia is another feature of Parkinsonism. It is the poverty (reduction in amount) of movement. How does bradykinesia present across the body? - Hypophonia (soft speech) - Hypomimia (paucity of blinking/ mask-like face) - Arms: Decremental bradykinesia, reduced arm swing when walking, micrographia - Legs: Smaller stride and festinant/Parkinsonian gait Stride and gait abnormalities would make

Answer 108

Resting tremors is the last of the 3 features of Parkinsonism. What are the diff types of tremors and their root cause? - Resting tremors - PD - Intention tremors - cerebellar - Postural tremors - benign essential A postural tremor, also sometimes referred to as an action tremor, is the term used to describe involuntary movement occurring when an individual holds a physical position against gravit

Answer 109

"Outline the causes of Parkinsonism - Idiopathic Parkinson Disease - Neuroleptic Medication - Wilson Disease - Parkinson plus syndromes - Infective encephalitis - Vascular Parkinsonism (Multi-infarct dementia from malignant HTN) But the presentation of this syndrome doesn't mean the patient definitely has Parkinson disease. Therefore we have to exclude the others: Neuroleptic medications (possible

Answer 110

"Outline the causes of Parkinsonism - Idiopathic Parkinson Disease - Neuroleptic Medication - Wilson Disease - Parkinson plus syndromes - Infective encephalitis - Vascular Parkinsonism (Multi-infarct dementia from malignant HTN) But the presentation of this syndrome doesn't mean the patient definitely has Parkinson disease. Therefore we have to exclude the others: Neuroleptic medications (possible

Answer 111

"Outline the causes of Parkinsonism - Idiopathic Parkinson Disease - Neuroleptic Medication - Wilson Disease - Parkinson plus syndromes - Infective encephalitis - Vascular Parkinsonism (Multi-infarct dementia from malignant HTN) But the presentation of this syndrome doesn't mean the patient definitely has Parkinson disease. Therefore we have to exclude the others: Neuroleptic medications (possible

Answer 112

What is Parkinson's Disease? progressive movement disorder marked by degeneration of dopamine producing neurons of the substantia niagra Assuming that all other causes of Parkinsonsim are ruled out, we would get to the final one: Idiopathic Parkinson's Disease. Or u can follow this definition. Same same la

Answer 113

Outline the various clinical manifestations of Parkinson's disease (vvvvvv IMPT!!!) Motor symptoms: - Bradykinesia - Hypophonia, Hypomimia, Mask-like expression, Decremental Micrographia, Festinant Gait/ Parkinsonian Gait, Retropulsion - Resting tremor - Lead-pipe/cogwheel rigidity Non-motor symptoms: - Psychiatric, Depression, Dementia, Mild cognitive impairment - Sleep/fatigue, REM sleep disorde

Answer 114

Outline the various clinical manifestations of Parkinson's disease (vvvvvv IMPT!!!) Motor symptoms: - Bradykinesia - Hypophonia, Hypomimia, Mask-like expression, Decremental Micrographia, Festinant Gait/ Parkinsonian Gait, Retropulsion - Resting tremor - Lead-pipe/cogwheel rigidity Non-motor symptoms: - Psychiatric, Depression, Dementia, Mild cognitive impairment - Sleep/fatigue, REM sleep disorde

Answer 115

"Treatment for Parkinson's Disease (vvvvvvvvvvv IMPT!!) What does treatment of Parkinson's Disease aim towards? What is the gold standard? re-dressing the dopamine deficit. Gold standard treatment is L-DOPA. But why not just give DOPA? Why got the L infront? Dopamine too large to cross BBB, will hang around in circulation doing everything else except getting into the brain Ok so we give L-DOPA. Bu

Answer 116

"Treatment for Parkinson's Disease (vvvvvvvvvvv IMPT!!) What does treatment of Parkinson's Disease aim towards? What is the gold standard? re-dressing the dopamine deficit. Gold standard treatment is L-DOPA. But why not just give DOPA? Why got the L infront? Dopamine too large to cross BBB, will hang around in circulation doing everything else except getting into the brain Ok so we give L-DOPA. Bu

Answer 117

"Treatment for Parkinson's Disease (vvvvvvvvvvv IMPT!!) What does treatment of Parkinson's Disease aim towards? What is the gold standard? re-dressing the dopamine deficit. Gold standard treatment is L-DOPA. But why not just give DOPA? Why got the L infront? Dopamine too large to cross BBB, will hang around in circulation doing everything else except getting into the brain Ok so we give L-DOPA. Bu

Answer 118

Other things that might be Parkinson's Disease. Just read below first. Make the cards next time.

Answer 119

"Horner's Syndrome is a failure of the sympathetic system. Symptoms would include: (PMA!!!) - Ptosis (partial, because 50% of the LPS is controlled by CN III) - Miosis - Anhidrosis - Reduced HR Assuming that there is TOTAL FAILURE of the sympathetic system, the symptoms mentioned above would be throughout the entire body. Otherwise it can be localised to a lesion. Localised causes of Horner's (eg

Answer 120

"Horner's Syndrome is a failure of the sympathetic system. Symptoms would include: (PMA!!!) - Ptosis (partial, because 50% of the LPS is controlled by CN III) - Miosis - Anhidrosis - Reduced HR Assuming that there is TOTAL FAILURE of the sympathetic system, the symptoms mentioned above would be throughout the entire body. Otherwise it can be localised to a lesion. Localised causes of Horner's (eg

Answer 121

Hx of ileum removal due to discovery of tumour Regular follow up shows no recurrence Otherwise healthy and eating well What does the DCML carry (sensory)? - Proprioception (conscious) and Vibration - Fine touch What is unconscious proprioception carried by? Spinocerebellar tract. What are the 3 components of the Romberg test (balance)? How many do we need to stay upright? - Vision (CNII) - Vestibu

Answer 122

Hx of ileum removal due to discovery of tumour Regular follow up shows no recurrence Otherwise healthy and eating well What does the DCML carry (sensory)? - Proprioception (conscious) and Vibration - Fine touch What is unconscious proprioception carried by? Spinocerebellar tract. What are the 3 components of the Romberg test (balance)? How many do we need to stay upright? - Vision (CNII) - Vestibu

Answer 123

What is InterNuclear Opthalmoplegia (INO)? These are lesions in the medial longitudinal fasciculus (MLF), where there is the inability of the ipsilateral eye to adduct on sideward gaze. However, if the MLF is only slowed (like demyelination), then you'll only get partial INO (eye adducts slowly). If you want to think about it, then just remember that left FEF >> right PPRF >> left MLF to get to th

Answer 124

Guillain-Barre Syndrome (form of peripheral neuropathy, meaning its LMN) Compared to botulinism/ other forms of paralysis, GBS is a form of ascending paralysis. It can occur (time) quickly, from days to weeks. Pathogenesis of GBS secondary to bacterial infection? Cross-reactivity (aka molecular mimicry) between Campylobacter jejuni proteins and axolemma. There are other causes of GBS but it's clos

Answer 125

Guillain-Barre Syndrome (form of peripheral neuropathy, meaning its LMN) Compared to botulinism/ other forms of paralysis, GBS is a form of ascending paralysis. It can occur (time) quickly, from days to weeks. Pathogenesis of GBS secondary to bacterial infection? Cross-reactivity (aka molecular mimicry) between Campylobacter jejuni proteins and axolemma. There are other causes of GBS but it's clos

Answer 126

Guillain-Barre Syndrome (form of peripheral neuropathy, meaning its LMN) Compared to botulinism/ other forms of paralysis, GBS is a form of ascending paralysis. It can occur (time) quickly, from days to weeks. Pathogenesis of GBS secondary to bacterial infection? Cross-reactivity (aka molecular mimicry) between Campylobacter jejuni proteins and axolemma. There are other causes of GBS but it's clos

Answer 127

What is the main issue with using antibiotics in CNS infections? The BBB prevents entry of Ig, complement and antibiotics. Need right antibiotic choice and dosing to ensure adequate penetration across BBB.

Answer 128

Bacterial meningitis is a medical emergency. What are the signs and symptoms? - generalised headache - neck stiffness - abnormal mental state / reduced conscious level - vomiting - non blanching rash (N. meningitidis) - Photophobia How to manage bacterial meningitis? - LP ASAP to obtain CSF, blood culture if fever present - Steroids before antibiotics (reduce inflammation --> reduce brain damage)

Answer 129

Bacterial meningitis is a medical emergency. What are the signs and symptoms? - generalised headache - neck stiffness - abnormal mental state / reduced conscious level - vomiting - non blanching rash (N. meningitidis) - Photophobia How to manage bacterial meningitis? - LP ASAP to obtain CSF, blood culture if fever present - Steroids before antibiotics (reduce inflammation --> reduce brain damage)

Answer 130

Bacterial meningitis is a medical emergency. What are the signs and symptoms? - generalised headache - neck stiffness - abnormal mental state / reduced conscious level - vomiting - non blanching rash (N. meningitidis) - Photophobia How to manage bacterial meningitis? - LP ASAP to obtain CSF, blood culture if fever present - Steroids before antibiotics (reduce inflammation --> reduce brain damage)

Answer 131

Bacterial meningitis is a medical emergency. What are the signs and symptoms? - generalised headache - neck stiffness - abnormal mental state / reduced conscious level - vomiting - non blanching rash (N. meningitidis) - Photophobia How to manage bacterial meningitis? - LP ASAP to obtain CSF, blood culture if fever present - Steroids before antibiotics (reduce inflammation --> reduce brain damage)

Answer 132

Cryptococcus neoformans meningitis tends to infect the immunocompromised, especially HIV Unlike bacterial meningitis, presentation is usually progressive. What are the presentations? - headache - neck stiffness uncommon - personality change and confusion (morer subtle than bacterial) - can progress to coma How to diagnosis cryptococcus neoformans meningitis? (IMPT!!!!!) - positive India ink in CSF

Answer 133

Cryptococcus neoformans meningitis tends to infect the immunocompromised, especially HIV Unlike bacterial meningitis, presentation is usually progressive. What are the presentations? - headache - neck stiffness uncommon - personality change and confusion (morer subtle than bacterial) - can progress to coma How to diagnosis cryptococcus neoformans meningitis? (IMPT!!!!!) - positive India ink in CSF

Answer 134

Tuberculous meningitis is most commonly associated with miliary TB. It can mimic acute bacterial meningitis, and is fatal within 5-8wks of onset if untreated. How to diagnose tuberculous meningitis? - AFB smear, AFB culture (gold standard) - TB PCR of CSF (low sensitivity, high specificity) Treatment? Rifampicin, Isoniazid, Pyrazinamide and Ethambutol Recall that MTB culture takes 6-8wks but this

Answer 135

What are the common causes of viral meningitis? - Enterovirus, Coxsackie virus - Mumps if non-immune - HSV - VZV - EBV, CMV - Basically all the viruses can hit the meninges/ parenchyma Presentation? headache, photophobia, neck stiffness, (rash) (meningitis symptoms)) Diagnosis? Why no culture? PCR. Culture 7-10 days, and viral culture very troublesome, need living cells Management? Supportive cuz

Answer 136

Outline the profiles of CSF in various types of CNS infections (IMPT!!!) Bacterial WCC in CSF: Polymorphonucleocytes (e.g neutrphils) Glucose in CSF: Low (consumed) Protein in CSF: High Viral WCC in CSF: Lymphocytes Glucose in CSF: normal (virus nth to do w glucose) Protein in CSF: elevated Fungal/TB/Treated bacterial WCC in CSF: Lymphocytes Glucose in CSF: low (consumed) Protein in CSF: elevated

Answer 137

What are mosquito borne (Arbovirus) causes of encephalitis? Eastern equine encephalitis Western equine encephalitis Venezuelan equine encephalitis St. Louis encephalitis West Nile encephalitis Japanese encephalitis Diagnosis? Serology +/- PCR If JE, nth much we can do. Supportive treatment.

Answer 138

Rabies are from rabid dogs, bats, and has a near 100% mortality What are the 2 classical symptoms of rabies? hydrophobia + autonomic dysfunction

Answer 139

What are some causes of viral encephalitis? Which 2 should be treated directly? (same suspects as viral meningitis) - HSV-1 (Give acyclovir ASAP) - HSV-2 (Give acyclovir ASAP) - Mumps - Measles - HHV6 (Human Herpes virus) - CMV - EBV - Enterovirus Can they be treated? Yep. Acyclovir (and Ganciclovir) What are the symtoms of viral encephalitis? - hallucinations - repetitive higher motor activity eg

Answer 140

What are some causes of viral encephalitis? Which 2 should be treated directly? (same suspects as viral meningitis) - HSV-1 (Give acyclovir ASAP) - HSV-2 (Give acyclovir ASAP) - Mumps - Measles - HHV6 (Human Herpes virus) - CMV - EBV - Enterovirus Can they be treated? Yep. Acyclovir (and Ganciclovir) What are the symtoms of viral encephalitis? - hallucinations - repetitive higher motor activity eg

Answer 141

What are some causes of viral encephalitis? Which 2 should be treated directly? (same suspects as viral meningitis) - HSV-1 (Give acyclovir ASAP) - HSV-2 (Give acyclovir ASAP) - Mumps - Measles - HHV6 (Human Herpes virus) - CMV - EBV - Enterovirus Can they be treated? Yep. Acyclovir (and Ganciclovir) What are the symtoms of viral encephalitis? - hallucinations - repetitive higher motor activity eg

Answer 142

What are the sources of initial infection for brain abscesses? Which one most common? - Direct spread from middle ear, frontal sinus or dental infection (poor dental hygiene, which is the commonest source) - Bacteraemia from deep seated infections (eg. infective endocarditis) - Iatrogenic (neurosurgical procedure)(Rare) What is the most common pathogen? The rest just read - Mouth flora --> Strepto

Answer 143

What are the sources of initial infection for brain abscesses? Which one most common? - Direct spread from middle ear, frontal sinus or dental infection (poor dental hygiene, which is the commonest source) - Bacteraemia from deep seated infections (eg. infective endocarditis) - Iatrogenic (neurosurgical procedure)(Rare) What is the most common pathogen? The rest just read - Mouth flora --> Strepto

Answer 144

What are the sources of initial infection for brain abscesses? Which one most common? - Direct spread from middle ear, frontal sinus or dental infection (poor dental hygiene, which is the commonest source) - Bacteraemia from deep seated infections (eg. infective endocarditis) - Iatrogenic (neurosurgical procedure)(Rare) What is the most common pathogen? The rest just read - Mouth flora --> Strepto

Answer 145

What are A-F? A: Hydrocephalus B: Encephalitis C: Meningitis D: Venous thrombosis E: Arterial vasospasm F: Microabscesses

Answer 146

Do not delay CT to get LP in cases unless there is just low grade fever/ non-sinister symptoms. Then only LP would be indicated.

Answer 147

Imaging: Role of Imaging in CNS infection: To rule out conditions Imaging modality of choice: MRI brain with contrast What are the systemic clues to look for? Progressive/ acute, immunocompromised, others Viral vs bacterial vs fungal infection: CSF, glucose, leukocyte types Classification of CNS infections: Congenital or acquired (source, location and causation) Complications of CNS infections: Me

Answer 148

Imaging: Some things for you to look through; HSV encephalitis

Answer 149

Imaging: Presentations that suggest congenital CMV: 1. Periventricular calcifications (VERY COMMON SPOT FOR CMV) 2. Neuronal migration disorders 3. Ventriculomegaly 4. WM signal abnormalities 5. Anterior temporal cysts 6. Patchy WM disease predominating in parietal lobes + anterior temporal cysts + ventriculomegaly would suggest CMV 80% of the time However, CMV-related WM disease is not progressiv

Answer 150

Imaging: Presentations that suggest congenital CMV: 1. Periventricular calcifications (VERY COMMON SPOT FOR CMV) 2. Neuronal migration disorders 3. Ventriculomegaly 4. WM signal abnormalities 5. Anterior temporal cysts 6. Patchy WM disease predominating in parietal lobes + anterior temporal cysts + ventriculomegaly would suggest CMV 80% of the time However, CMV-related WM disease is not progressiv

Answer 151

Imaging: CMV infections would have different presentations based on time of infection. First Trimester Severe microcephaly Lissencephaly (small and smooth) Ventriculomegaly Leukoencephalopathy Intracranial calcifications Second Trimester Polymicrogyria Schizencephaly (wrinkly and wrong location) Ventriculomegaly Leukoencephalopathy Intracranial calcifications Third Trimester Ventriculomegaly Leuko

Answer 152

Imaging: CMV infections would have different presentations based on time of infection. First Trimester Severe microcephaly Lissencephaly (small and smooth) Ventriculomegaly Leukoencephalopathy Intracranial calcifications Second Trimester Polymicrogyria Schizencephaly (wrinkly and wrong location) Ventriculomegaly Leukoencephalopathy Intracranial calcifications Third Trimester Ventriculomegaly Leuko

Answer 153

Imaging: What are the congenital CNS infections that you know of? TORCH What are the clinical findings suggestive of congenital CNS infection? Calcifications at different places would mean different things What are the expected imaging findings? Microcephaly, neuronal migration issues etc Can we time the injury/infection? We can for CMV Why is it important to diagnose congenital CMV infection post

Answer 154

Imaging: Ring enhancing lesions Read below

Answer 155

Imaging: Neonatal infections Most common bacterial infection: GBS and E. coli Other important infective agents: Listeria, Citrobacter, Enterobacter Read S/s and whatnot below. Listeria also in pregnancy and immunocompromised!

Answer 156

We all know that the main treatment for Parkinson's would be L-DOPA and CARBIDOPA, but what are the others? Dopamine agonists (young patients): - Rotigotine - Ropinorole - Pramipexole - Amantadine MAO(B) inhibitors (older patients, use as adjuncts): - Rasagiline - Selagiline COMT inhibitors (older patients, use as adjuncts): - Entacapone - Tolcapone Mn: Prami picks oil Amanda Dines MAO-B acts on d

Answer 157

We all know that the main treatment for Parkinson's would be L-DOPA and CARBIDOPA, but what are the others? Dopamine agonists (young patients): - Rotigotine - Ropinorole - Pramipexole - Amantadine MAO(B) inhibitors (older patients, use as adjuncts): - Rasagiline - Selagiline COMT inhibitors (older patients, use as adjuncts): - Entacapone - Tolcapone Mn: Prami picks oil Amanda Dines MAO-B acts on d

Answer 158

We all know that the main treatment for Parkinson's would be L-DOPA and CARBIDOPA, but what are the others? Dopamine agonists (young patients): - Rotigotine - Ropinorole - Pramipexole - Amantadine MAO(B) inhibitors (older patients, use as adjuncts): - Rasagiline - Selagiline COMT inhibitors (older patients, use as adjuncts): - Entacapone - Tolcapone Mn: Prami picks oil Amanda Dines MAO-B acts on d

Answer 159

What would this be? Cerebral infarction Something similar came out for 2019/2020 M2 Pros MEQ. Note the signs of acute infarction in the picture above, namely hypodense brain parenchyma. Also note that the ventricles can be compressed by infarctions, might be due to gliosis (neuronal equivalent of non-CNS fibrosis).

Answer 160

What is a reflex arc made of? Afferent limb (sensory neuron) + efferent limb (LMN) What are the physiological functions of the reflex arc? - Prevents overstretching of muscle - protective - Helps maintain posture - Generates tone UMN input modulates and regulates reflex.

Answer 161

"CNS NOT. BOTH. Spinal cord lesion is both UMN and LMN, but spinal cord lesion itself is CNS. rmb this? ""Ehhhh one thing to note is that some questions would ask if it's CNS/PNS instead of LMN/ UMN. If it's UMN/LMN then the answer would be both, but if it's CNS then it would just be CNS."""

Answer 162

Homonymous hemianopia. CNS (likely optic tract)

Answer 163

Anterior cord syndrome results in - Loss of pain & temperature - Loss of crude touch & pressure - UMN weakness Causes: Cord Infarcts. Propensity for infarct because anterior spinal artery is the ONLY supply to anterior spinal cord Posterior cord syndrome results in - Loss of proprioception and vibration - Loss of fine touch - UMN weakness Causes: Tabes Dorsalis (syphilis), B12 (folate) deficiency

Answer 164

"CNS or PNS? CNS cuz hyperreflexia, hypertonia, upgoing plantars, ankle clonus, Brain or Cord? Cord @ thoracic level What if it was areflexia and hypotonia? CNS or PNS? PNS ""Clonus is a series of involuntary, rhythmic, muscular contractions, and relaxations. It may be caused by interruption of the UMN fibers such as stroke, multiple sclerosis, or by metabolic alterations such as severe hepatic fa

Answer 165

D Cauda equina no longer nerve bodies, consists of roots. Hence considered LMN --> areflexia and hypotonia (downgoing plantars)

Answer 166

CNS or PNS? CNS. R pronator drift, hyperreflexia, hypertonia Brain or Cord? Left Brain, contralateral so right sided sign means left brain Which part of the Brain? Cerebral hemispheres or brainstem. Not cerebellum cuz that would be pure ataxia If patient has double vision and vertigo? Brainstem. Gaze centre and cerebellar connections got hit If patient has dysphasia? (NOT DYSPHAGIA) Cortical (grey

Answer 167

CNS or PNS? CNS Brain or Cord? Brain. Unilateral Which part of the brain? Brainstem Exact lesion location? Right pons. Hits CN7 motor nerves (paralysis of both upper and lower half of ipsilateral right face), hits corticospinal (descending) tract (left side UMN arm & leg weakness) Motor cranial nerves analogous to LMN!! Revision Corticobulbar tract to muscles on lower face receive only contralater

Answer 168

NMJ and Muscle lesions What are signs of proximal myopathy (muscle lesions)? - Proximal weakness - Wasting without fasciculations - +/- Pseudohypertrophy What are signs of NMJ lesions? - Proximal weakness - Ocular weakness (think myasthenia gravis) - Fatiguability (think myasthenia gravis) Why does NMJ and muscle lesions both present with proximal weakness? Why not distal? Proximal muscles exert m

Answer 169

NMJ and Muscle lesions What are signs of proximal myopathy (muscle lesions)? - Proximal weakness - Wasting without fasciculations - +/- Pseudohypertrophy What are signs of NMJ lesions? - Proximal weakness - Ocular weakness (think myasthenia gravis) - Fatiguability (think myasthenia gravis) Why does NMJ and muscle lesions both present with proximal weakness? Why not distal? Proximal muscles exert m

Answer 170

Duchenne muscular dystrophy (DMD) is a X-linked genetic disorder characterized by progressive muscle degeneration and weakness. Which gene is mutated in DMD? Dystrophin gene on X chromosome. Dystrophin is a component of the membrane cytoskeleton in normal muscle, contributes to membrane stability. What does DMD patients present with? - Proximal weakness - Affect heart and respiratory muscles (deat

Answer 171

General observations about LMN (roots, plexus and nerve) Are part of LMN, so will have areflexia, hypotonia, wasting, fasciculations, weakness, sensory abnormalities General observation about nerves Long nerves more vulnerable to systemic insults than short nerves. Henceit affects the extremities of limbs first (glove and stocking distribution weakness and numbness) (all 4 limbs, but usually feet

Answer 172

Hx of ileum removal due to discovery of tumour Regular follow up shows no recurrence Otherwise healthy and eating well What does the DCML carry (sensory)? - Proprioception (conscious) and Vibration - Fine touch What is unconscious proprioception carried by? Spinocerebellar tract. What are the 3 components of the Romberg test (balance)? How many do we need to stay upright? - Vision (CNII) - Vestibu

Answer 173

Guillain-Barre Syndrome (form of peripheral neuropathy, meaning its LMN) Compared to botulinism/ other forms of paralysis, GBS is a form of ascending paralysis. It can occur (time) quickly, from days to weeks. Pathogenesis of GBS secondary to bacterial infection? Cross-reactivity (aka molecular mimicry) between Campylobacter jejuni proteins and axolemma. There are other causes of GBS but it's clos

Answer 174

"Outline the differences between syncope and seizure (fit) (vvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvv IMPT!!! Just memorize this table) Think predisposition, preceding features, preceding vocalization, breathing, twitching, duration and then common traits. Syncope predisposed by vagal stimulation (peripheral vasodilation), fasting/dehydration and happens when pt is upright. Seizure predisposed by

Answer 175

"Other features of sinister headaches A thunderclap headache, also referred to as a lone acute severe headache, is a headache that is severe and sudden-onset. Which causes of thunderclap headaches are sinister and must be excluded? (""VSD"") (IMPT!!!!) - Subarachnoid haemorrhage!!!! - Venous sinus thrombus - Dissection Which causes of thunderclap headaches are non-sinister (primary headaches) and

Answer 176

"Temporal tenderness/Jaw claudication (headache pain on chewing) is a sign of temporal arteritis, a sinister headache Why is it important to diagnose immediately? If missed, causes bilateral blindness in 50% of untreated patients!!! Definitive test for temporal arteritis? Temporal artery biopsy (but beware of skip lesions) If headache in elderly patient, suspect temporal arteritis and just prescri

Answer 177

Small ring enhancing lesions with microabsesses points towards? pyogenic CNS infections

Answer 178

What is TORCH? What does TORCH stand for? TORCH refers to a group of infectious agents that can cause infection of a developing fetus or newborn Toxoplasmosis Others (syphilis, ZIKA) Rubella CMV HSV ZIKA and CMV most impt!!! Periventricular calcifications = CMV Craniofacial disproportion and redundant scalp skin in the occipital region = ZIKA ]

Answer 179

2 main features of congenital infection that suggests 1st trimester exposure? - Severe microcephaly - Lissencephaly 2nd trimester exposure? - Polymicrogyria - Schizencephaly General rule is earlier = harder to infect but more severe later = easier to infect but less severe

Answer 180

What are the most common causes of pyogenic CNS infection in neonates? Grp B Strep (S. agalactiae) & E. Coli Why infection from enteric organisms is more prevalent in the first two weeks of life? Maternal antibodies against coliform organism do not cross the placenta. Hence, there is a lack of passive immunity against gram-negative organisms. What are other important infective agents in neonatal p

Answer 181

Describe the 2 photoreceptors in the eyes (IMPT!!!!) Rods are for scotopic vision. Most sensitive to dim light and do not convey sense of color Cones are for photopic vision. Work in bright light, responsible for acute detail, black and white and colour vision Which one is concentrated in fovea and which one is absent in fovea? Fovea all cones!!! TLDR cones are colourful and likes to gather in fov

Answer 182

Name 3 differences between rods and cones (vvvvvv IMPT!!!) TLDR - Rods for monochromatic vision, has good sensitivity and is distributed throughout the retina - Cones for colour vision, has poor sensitivity and is found mainly in the fovea There are 120M rods but only 6M cones per eye

Answer 183

name some causes of night blindness (nyctylopia) - Vit A deficiency - Retinitis pigmentosa (retinal issues) name some causes of color blindness - Congenital (red-green, X-linked) - Optic Neuropathy

Answer 184

Outline and draw the basic visual pathway (vvvvvvvvvvvvvvvvvvv IMPT!!!!) Retina Optic nerve Optic chiasma (nasal retinal fields would decussate) Optic tract Lateral geniculate nucleus (Thalamus) Optic radiation Primary visual cortex (at occipital lobe) Underlined ones are where synapses exist. The optic radiation is made up of 2 halves; the superior (Baum's) loop and inferior (Meyer's) loop. Baums

Answer 185

What are the lesions that are associated to damage at different locations? (vvvvvvvvvvvvvvvvvvv IMPT!!!) Optic nerve: monocular blindness Optic chiasm: bitemporal hemianopia Optic tract: homonymous hemianopia Optic radiation: homonymous quadrantanopia Ocular cortex: homonymous hemianopia with macular sparing Why don't people notice that they can have deficiencies in sight? 2/3 of our visual fields

Answer 186

What are the lesions that are associated to damage at different locations? (vvvvvvvvvvvvvvvvvvv IMPT!!!) Optic nerve: monocular blindness Optic chiasm: bitemporal hemianopia Optic tract: homonymous hemianopia Optic radiation: homonymous quadrantanopia Ocular cortex: homonymous hemianopia with macular sparing Why don't people notice that they can have deficiencies in sight? 2/3 of our visual fields

Answer 187

Rod photoreceptors Rods are for scotopic vision. Most sensitive to dim light and do not convey sense of color Cones are for photopic vision. Work in bright light, responsible for acute detail, black and white and colour vision Perfect visual acuity = can focus very well = cornea + lens ok! Colour vision ok = cones ok = fovea/macula ok Can perfectly in day = optic nerve ok Cannot see in dark = rods

Answer 188

"Left occipital lobe Right visual field cannot see = left kena hit. Homonymous Hemianopia = after optic chiasma = optic tract/occiptal lobe (if w macula sparing) Homonymous Quadrantanopia = optic radiation Pt might say ""right eye cannot see"". If test, then they will realize its right field gone, not right eye problem. Tbh just draw out la HAHAHHA then sure wont get wrong"

Answer 189

Abducens nerve binocular diplopia = both eyes not looking at the same direction. Think about what keeps the eyes looking in the same direction!! So extraocular muscles, CN3/4/6 and its nuclei, brainstem structures (MLF,etc). Temporal lobe hit = Meyer's loop hit = Homonymous Superior Quadrantanopia

Answer 190

What is the tonotopicity of cochlear hair cells? - Higher sounds (Hz) nearer the oval and round windows (outside) - Lower sounds (Hz) nearer the end of the cochlea (inside) How is sound amplified? What protects us from loud noises? Amplification of sound is by the middle ear (tympanic membrane) and outer ear. Muscles like the stapedius and tensor tympani protect you from loud noises What are the 2

Answer 191

What is the tonotopicity of cochlear hair cells? - Higher sounds (Hz) nearer the oval and round windows (outside) - Lower sounds (Hz) nearer the end of the cochlea (inside) How is sound amplified? What protects us from loud noises? Amplification of sound is by the middle ear (tympanic membrane) and outer ear. Muscles like the stapedius and tensor tympani protect you from loud noises What are the 2

Answer 192

What is the tonotopicity of cochlear hair cells? - Higher sounds (Hz) nearer the oval and round windows (outside) - Lower sounds (Hz) nearer the end of the cochlea (inside) How is sound amplified? What protects us from loud noises? Amplification of sound is by the middle ear (tympanic membrane) and outer ear. Muscles like the stapedius and tensor tympani protect you from loud noises What are the 2

Answer 193

Outline the results of Rinne's and Weber's Tests in the 2 main diff types of hearing loss. (IMPT!!!!) Conductive hearing loss (noise induced, otitis media, etc) Rinne: Bone louder than air (bone bypass outer/middle ear lesion) Weber: Lesion side louder (background noise shielded by outer/middle ear lesion)) Sensorineural hearing loss (problem in inner ear/CN VIII) Rinne: Air louder than bone (both

Answer 194

Noise induced hearing loss (inner ear) Cerumen (ear wax) = outer ear Noise induced hearing loss = inner ear Chronic suppurative otitis media = middle ear Otitis externa = outer ear Perforated ear drum = middle/outer ear Air conduction > bone conduction = sensorineural hearing loss = inner ear/CN VII lesion Weber localize to left = left louder --> consider sensorineural --> left normal, right side

Answer 195

Outline the results of Rinne's and Weber's Tests in the 2 main diff types of hearing loss. (IMPT!!!!) Conductive hearing loss (noise induced, otitis media, etc) Rinne: Bone louder than air (bone bypass outer/middle ear lesion) Weber: Lesion side louder (background noise shielded by outer/middle ear lesion)) Sensorineural hearing loss (problem in inner ear/CN VIII) Rinne: Air louder than bone (both

Answer 196

Frusemide Frusemide = Loop diuretic Metformin = Insulin sensitizer Perindopril = ACE inhibitor Candesartan = AGII T1 receptor blockers Simvastatin = HMG CoA Reductase inhibitor Revision: drugs that causes ototoxicity - Aminoglycosides - Quinine - Loop Diuretics - Chemotherapeutic Drugs - Local Anesthetic

Answer 197

What is dysphasia? Disorder of language. - Wernicke hit = Fluent/Receptive Aphasia - Broca hit = Non-Fluent/Expressive Aphasia What is Dysarthria? Disorder of articulation (weak speech muscles) Also read up on developmental assessment. Sometimes a child may seem like he/she has developmental problem but actually it can be normal if u consider their family backgrounds

Answer 198

Pt can talk very well but doesnt make sense. Where is the lesion? Left parietal cortex Can talk very well --> not broca's --> not expressive aphasia --> so its fluent/receptive aphasia (wernickes) Wernicke's normally at left temporal/parietal cortex (angular gyrus). Broca's normally at left frontal cortex. Wrenicke and Broca normally both on the left. Even for right handers (50-70% still on the le

Answer 199

Sleep hygeine: what are some tips for achieving better sleep!!! - Maintain a regular bed and wake time schedule, including weekends - Establish a regular, relaxing bedtime routine - Create a sleep-conducive environment that is dark, quiet, & comfortable - Sleep on a comfortable mattress and pillows - Do not work or surf the internet in bed - Turn off e-devices when you want to sleep. - Avoid alcoh

Answer 200

What are the two major processes (not only these 2, but these 2 are the biggest) that determine when you feel sleepy? - Homeostatic sleep drive (longer you awake, the bigger sleep pressure) - Circadian sleep drive (increases during nighttime hour. in evening it actually gives high alertness pressure to oppose sleep homeostat!) Sleep homeostat basically means that you're tired, where sleep pressure

Answer 201

Outline the 3 different states of sleepwake behaviour 1. Wakefulness: Aware of onset and environment, cerebral cortex is active 2. REM sleep: Unconscious, but the celebral cortex is active. Skeletal muscles are mostly paralysed. Dreams occur and there is saccadic eye movement. 3. Non-REM sleep (N1, N2, N3): Unconscious, with reduced cortical activity. Reduced muscle tone. Which stage does dreams o

Answer 202

7 Stay up more than 21 hours is equivalent to being drunk ok! Dont play play.

Answer 203

D Woman you sound like a year 2 medical student Nap not advised. Will decrease homeostatic sleep pressure if nap too much The phone is the problem. Remove it

Answer 204

What are the predominant neurotrasmitters involved in stress? NE, Serotonin, Dopamine Where are the key structure in stress response in the brain? amygdala, Hypothalamus, Locus coeruleus, Cerebellum

Answer 205

What are the 2 major effects of chronic stress on the brain and body? - Depression and reduced hippocampal volume - Metabolic syndrome

Answer 206

Name examples of things that upregulate and downregular neurogenesis (IMPT!!!) Up-regulation: 1. Enriched environment 2. Exercise 3. Learning 4. Oestrogen 5. Antidepressant drugs Down-regulation: 1. Stress 2. Glucocorticoid 3. Age 4. Opiates 5. Excitatory amino acids How to be smarter: Exercise, learn in enriching enviroment, be a girl, spam AD drugs How to NOT be smarter: Stress, aging, spam gluc

Answer 207

Name examples of things that upregulate and downregular neurogenesis (IMPT!!!) Up-regulation: 1. Enriched environment 2. Exercise 3. Learning 4. Oestrogen 5. Antidepressant drugs Down-regulation: 1. Stress 2. Glucocorticoid 3. Age 4. Opiates 5. Excitatory amino acids How to be smarter: Exercise, learn in enriching enviroment, be a girl, spam AD drugs How to NOT be smarter: Stress, aging, spam gluc

Answer 208

Exercise How to be smarter: Exercise, learn in enriching enviroment, be a girl, spam AD drugs How to NOT be smarter: Stress, aging, spam glucocorticoid, spam opiates

Answer 209

"Benzodiazepines are the most commonly used anti-anxiety and ""hypnotic"" agents (sleeping pills for insomnia) to treat the symptoms and behaviors caused by anxiety disorders. Name the different benzodiazepines. short acting: midazolam intermediate acting: lorazepam, alprazolam longer acting: diazepam What is the MoA of Benzodiazepines? BZD binds to specific BZD sites in the CNS and potentiates GA

Answer 210

"Benzodiazepines are the most commonly used anti-anxiety and ""hypnotic"" agents (sleeping pills for insomnia) to treat the symptoms and behaviors caused by anxiety disorders. Name the different benzodiazepines. short acting: midazolam intermediate acting: lorazepam, alprazolam longer acting: diazepam What is the MoA of Benzodiazepines? BZD binds to specific BZD sites in the CNS and potentiates GA

Answer 211

Name some adverse effects of benzodiazepine (Xanax) (vvvvvvvvvvvv IMPT!!!!) - CNS: increase drowsiness, decrease motor skills, increase reaction time, sedation (frequent) - CNS: Anterogade amnesia. Memory disturbances are particularly profound after intravenous sedation (frequent) - CVS: decreased BP, respiratory depression in predisposed patients. (frequent) - Paradoxical effects: excitement, gar

Answer 212

"Name some non-benzodiazepine hypnotics. What is their MoA? Zolpidem, Zopiclone. Act on BZD sites similar to BZD Short elimination T1/2 with hypnotic effects comparable to benzodiazepines. So these drugs are only used for insomnia. ""the zzzzzz drug"" Less side effects than benzodiazepines. Main side effect are withdrawl and abuse potential!"

Answer 213

What is the biochemical basis behind antidepressants? Replenish deficiency of monoamines

Answer 214

Name some of the effects of depression - Poor mood - Loss of interest - Appetite changes - Reduced concentration and energy - Feelings of shame and guilt - Suicidal ideation - Less or more sleep - Psychomotor retardation Symptoms persist for >2 weeks + severity of symptoms interfere with normal functioning

Answer 215

"Name the 4 classes of commonly used antidepressants. Which 2 are commonly used? Give examples of each. 1. Selective Serotonin Re-uptake Inhibitors (SSRIs) (e.g fluoxetine, escitalopram, sertraline, paroxetine) 2. TriCyclic Antidepressants (TCAs) (amitriptyline, imipramine) 3. Serotonin norepinephrine reuptake inhibitors (SNRIs) 4. Noradrenergic selective serotonin antidepressant (NaSSa) depressed

Answer 216

MOA of SSRI? inhibit reuptake of serotonin at synapse. Creates excessive/ increased neurotransmitters in the synapse. Examples of SSRI that are used? 1. Fluoxetine (Prozac) 2. Escitalopram (Laxapo) 3. Sertraline 4. Paroxetine Increasing neurotrasmitters can increase BDNF --> neurogenesis

Answer 217

What are the adverse effects of SSRIs? (IMPT!!!!) - Anxiety - Weight gain - Headache, nausea (first few days) - Sexual dysfunction - Hyponatremia - No fatality in overdose (similar to BZD) They are also very potent CYP450 enzyme inhibitors. Inhibition descends in the order Fluvoxamine > Fluoxetine > Paroxetine > :Sertraline > Escitalopram So SSRI anti-depressants can give u anxiety and weight gain

Answer 218

What are the adverse effects of TCAs? (IMPT!!!) - CNS effects: sedation, fatigue - Cardiac rhythm: tachycardia, arrhythmias - Postural hypotension - Anticholinergic effects: glaucoma, blurred vision, urinary retention, constipation Most importantly: Fatality in overdose. FATALITY IN OVERDOSE! DEPRESSED PPL'S WAY OF SUICIDE - this is unlike the others like SSRIs. So SSRIs are contraindicated in dep

Answer 219

"Psychosis is a severe mental disorder in which thought and emotions are so impaired that contact is lost with external reality. Schizophrenia is a subtype of psychosis. What is the hypothesis behind the pathophysiology of psychosis? Excessive dopamine transmission in mesocortico-limbic system. Its a hypothesis so antipsychotic drugs are used to treat symptoms, not cause. What are the positive sym

Answer 220

"Outline the classes of antipsychotic drugs and give examples of each (IMPT!!!) Typical (1st gen) - Chlorpromazine (low) - Haloperidol (high potency) (more extrapyramidal side effect) Atypical (2nd gen) (less Extrapyramidal side effect but weight gain + metabolic syndrome) - Risperidone (more extrapyramidal side effect) - Olanzapine - Quetiapine - Clozapine(agranulocytosis) - Aripipazole ""Mn - He

Answer 221

Difference between typical (1st gen) vs atypical (2nd gen) antipsychotic drugs PD? Typical blocks: D2 > 5-HT2 receptors - and also D1, cholinergic, histaminic, α adrenergic Atypical blocks: 5-HT2 > D2 - and a number of other receptors blocking D2 = more EPSE = higher risks of parkinsonism 5-HT2 is for anti-psychotics 5-HT3 is for nausea and vomiting 5-HT4 is for constipation oh gawd halp Serotonin

Answer 222

"Adverse effects of typical and atypical antipsychotic drugs? Typical: Haloperidol hgher potency than chlorpromazine, more EPSE Atypical: Generally have fewer EPSE than typical Clozapine: Agranulocytosis, weight gain and sedation Olanzapine: Weight gain and sedation Quetiapine: Weight gain Risperidone: EPS (dose dependant), weight gain Mn for the EPSE would be PAMAT The ""pine"" antipsychotics all

Answer 223

A Yup benzodiazepines can cause anterograde amnesia Benzodiazepines causes tolerance, dependance and withdrawal midazolam is the short acting one. Lorazepam intermediate acting, diazepam long acting. Benzodiazepines dont bind to dopaminertic receptors. Benzodiazepines binds to specific BZD sites in the CNS and potentiates GABA actions by increasing the frequency of chloride channel opening. It is

Answer 224

What are the 3 types/Stages of memory? (IMPT!!!!) 1. Sensory/very short-term/ temporary (Large capacity, short duration. REQUIRES ATTENTION!) 2. Short term/working (Limited capacity, short duration) 3. Long term memory (large capacity) They can vary in capacity, duration and function.

Answer 225

Short term memory primarily involves the hippocampus of the brain. Emotions primarily involve the amygdala of the brain. After information flows through the circuits many times links would stabilise and not need the hippocampus to bring the data together. These would then become part of long-term memory (enhanced with environment connections). Both are v nearby. So memory associated w emotions ten

Answer 226

Dementia is a clinical syndrome characterised by (IMPT!!!) - progressive global deterioration in cognitive function and memory - in a clear state of consciousness, - sufficiently severe to interfere with social and occupational function. Most cases of dementia are long-standing, and tests need to be done that are very sensitive and repeatable.

Answer 227

Name some early warning symptoms of dementia (IMPT!!!) - difficulty learning and retaining new information - language problems - difficulty handling complex tasks - alteration in behaviour - loss of reasoning ability - loss of spatial ability and orientation

Answer 228

Molecular imaging for Alzheimers looks for (vvvvvvv IMPT!!!) 1. Beta Amyloid plaques 2. Neurofibrillary tangles (tau proteins) Hippocampal atrophy!!! Do. Not. Biopsy. The. Brain!!! Use molecular imaging.

Answer 229

Prevention of dementia? (IMPT!!!!) - Lifestyle changes (An active, healthy and socially integrated lifestyle may prevent dementia) (social networks, mental activities, physical activity) - Healthy diet, stop smoking, stop alcohol - Reduce vascular risk - Reduce neuronal damage - Monitor blood pressure, obesity, blood cholesterol, diabetes - Enhances cognitive reserve - Reduce “stress” Key to slow

Answer 230

Possible treatments for dementia that are being tested? 1. AChEI 2. Memantine 3. Vitamin B (Wernicke's etc) 4. Ginkgo biloba 5. Statins, anti-HTN 6. Amyloid and tau proteins Know that treatment exist and are being tested.

Answer 231

E Alzheimer's associated with beta amyloid plaque and neurofibrillary tangles. vascular disease is a risk factor for dementia as well Treatments are available and being tested Atrophy is at hippocampus you should know by now that alzheimer is the most common cause of dementia, so they are used almost interchangeably

Answer 232

"Outline the differences between syncope and seizure (fit)! (vvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvv IMPT!!! Just memorize this table) Think predisposition, preceding features, preceding vocalization, breathing, twitching, duration and then common traits. Syncope predisposed by vagal stimulation (peripheral vasodilation), fasting/dehydration and happens when pt is upright. Seizure predisposed b

Answer 233

which are the 4 most impt systems in maintaining consciousness? (IMPT!!!) 1. Cardiovascular system 2. Respiratory system 3. Brain(CNS) function 4. Energy substrates and electrolytes TLDR, good bp, enough oxygen, enough glucose, suitable environment whack any of these = temporarily depressed cortical activity = pengsan/faint/syncope

Answer 234

Prolonged impairment of consciousness (comatose state) occurs if large areas of the brain is affected. Injury/insult to the brain persist depending on the cause Name some causes of comatose state - Traumatic brain injury - Cerebrovascular accident (Hemorrhage, Thrombosis, Embolism, Vasculitis) - CNS Infection (viral/autoimmune encephalitis) - Refractory status epilepticus and drugs. think about th

Answer 235

"""Fit vs Faint"" How to diagnose? (IMPT!!!) - Clinical: History is key. Based on detailed description of events experienced by the patient and/or eye-witness before, during and after a event/seizure (blow by blow) - Video-recording of event (gold standard lol) - (if not) Witness should attend consultation/be telephoned - (if not) Written account ""HH ah, how to diagnose Fit vs Faint clinically??"

Answer 236

"What are the investigations for (IMPT!!!) Syncope? - normally not investigated in young (hyperattenuated vagal systems) unless recurrent - then look for cardiac issues (ECG & 24hr holter monitoring) - and autonomic features (tilt table) Seizures? - Look for electrolyte abnormalities (renal panel) and infective precipitants (FBC, culture) - :then look for electrical abnormalities in the brain (EEG

Answer 237

Glasgow Coma Scale (GCS) is used to assess level of consciousness and it is comprised of 3 parts (E,V,M) 1. Eye-opening response 2. Best verbal response 3. Best motor response Outline some limitations of using the GCS (IMPT!!) - Evaluating eye opening if there is severe orbito-facial injury - Assessment of verbal function if intubated - Inability to score differences between right- and left-sided

Answer 238

Glasgow Coma Scale (GCS) is used to assess level of consciousness and it is comprised of 3 parts (E,V,M) 1. Eye-opening response 2. Best verbal response 3. Best motor response Outline some limitations of using the GCS (IMPT!!) - Evaluating eye opening if there is severe orbito-facial injury - Assessment of verbal function if intubated - Inability to score differences between right- and left-sided

Answer 239

C E - open eyes to pain = 2 V - moans incoherently = 2 M - right arm pull hand away = can localize pain = 5 E2 V2 M5 = 9.

Answer 240

What is the most common cause of acute stroke? (IMPT!!!) Ischaemic stroke (85%), normally seen in older patients (atherosclerosis, HTN etc) Which is the most dangerous type of stroke? SAH (always this guy) (25% die before reach ED), normally seen in younger patients (berry aneurysms/arteriovenous malformations) Are parenchymal strokes more serious or SAH? SAH What are the signs of acute stroke? -

Answer 241

What is the most common cause of acute stroke? (IMPT!!!) Ischaemic stroke (85%), normally seen in older patients (atherosclerosis, HTN etc) Which is the most dangerous type of stroke? SAH (always this guy) (25% die before reach ED), normally seen in younger patients (berry aneurysms/arteriovenous malformations) Are parenchymal strokes more serious or SAH? SAH What are the signs of acute stroke? -

Answer 242

Outline the risk factor for strokes. Which one is the strongest modifiable risk factor? (vvvvvvv IMPT!!!) 1. HTN (strongest modifiable risk factor for all strokes) 2. DM 3. High lipids 4. Smoking 5. AF rather standard answers but need to know because these are what we target in secondary prevention Just reducing BP by 9mmHg can reduce stroke risk by 44%!! Treatment for stroke from DM is harder tha

Answer 243

Why are stroke units important? improves outcomes!! Not a trivial card.

Answer 244

First line drug for stroke? IV t-PA (thrombolytic, only 1 med lol!! time to specialize in stroke??) Why should reasonable glycemic control be maintained in all acute stroke patients.? Hyperglycaemia associated with worse outcomes and increased risk of intracerebral haemorrhage in patients treated with t-PA (fibrinolytic) Why should measure be taken to combat fever in acute stroke patients? Fever i

Answer 245

First line drug for stroke? IV t-PA (thrombolytic, only 1 med lol!! time to specialize in stroke??) Why should reasonable glycemic control be maintained in all acute stroke patients.? Hyperglycaemia associated with worse outcomes and increased risk of intracerebral haemorrhage in patients treated with t-PA (fibrinolytic) Why should measure be taken to combat fever in acute stroke patients? Fever i

Answer 246

Should we treat HTN in patients with early ischemic stroke? No, unless hypertensive encephalopathy, myocardial ischemia, CHF, aortic dissection. Mild and moderately elevated BP not routinely lowered!! Reasons for not treating HTN? 1. Blood pressure returns to baseline in a few days 2. BP lowering can cause infarct extension because of presence of an ischaemic penumbra and loss of autoregulation Re

Answer 247

Should we treat HTN in patients with early ischemic stroke? No, unless hypertensive encephalopathy, myocardial ischemia, CHF, aortic dissection. Mild and moderately elevated BP not routinely lowered!! Reasons for not treating HTN? 1. Blood pressure returns to baseline in a few days 2. BP lowering can cause infarct extension because of presence of an ischaemic penumbra and loss of autoregulation Re

Answer 248

"How fast does tPA need to be administered in ischemic stroke? Why? Within 4.5hrs!! Time is brain, millions of neurons die per second!! ""The greatest changes to healthcare is not brilliant doctors but changes to systems"""

Answer 249

"How fast does tPA need to be administered in ischemic stroke? Why? Within 4.5hrs!! Time is brain, millions of neurons die per second! ""The greatest changes to healthcare is not brilliant doctors but changes to systems"""

Answer 250

Yes within 4.5hrs yo. He alr 3hrs in No haemorrhage is good (tPA contraindicated in haemorrhage) Normal glucose is good (hyperglycamia associated with worse outcomes and increased risk of ICH)

Answer 251

Future of stroke treatment Endovascular treatment of acute ischaemic stroke: - Merci Retriever - Stentrievers Treatment of malignant hemispheric infarction: - Decompressive surgery (release pressure through the skull). Early decompression yields better results

Answer 252

Parkinsonism is a clinical syndrome that is normally associated with? (IMPT!!!!!) 1. Lead pipe rigidity (lack of voluntary movement) 2. Bradykinesia (immobility) 3. Resting tremors What are some causes of Parkinsonism? (memorize all) - Idiopathic Parkinson's disease - Neuroleptic medication (EPSE - typical psychotics etc) - Wilson disease - Infective encephalitis - Vascular Parkinsonism - Parkinso

Answer 253

Parkinsonism is a clinical syndrome that is normally associated with? (IMPT!!!!!) 1. Lead pipe rigidity (lack of voluntary movement) 2. Bradykinesia (immobility) 3. Resting tremors What are some causes of Parkinsonism? (memorize all) - Idiopathic Parkinson's disease - Neuroleptic medication (EPSE - typical psychotics etc) - Wilson disease - Infective encephalitis - Vascular Parkinsonism - Parkinso

Answer 254

Lead-pipe rigidity is a feature of Parkinsonism. What is rigidity? Rigidity is the resistance to passive movement. How does extrapyramidal rigidity present vs UMN rigidity (hypertonia)? Lead-pipe (hard all the time) vs Clasp knife (easy in some planes of movement) In UMN rigidity (clasp knife), why is it resistance found in only some ranges of motion? - Certain sets of muscles are stronger than an

Answer 255

Lead-pipe rigidity is a feature of Parkinsonism. What is rigidity? Rigidity is the resistance to passive movement. How does extrapyramidal rigidity present vs UMN rigidity (hypertonia)? Lead-pipe (hard all the time) vs Clasp knife (easy in some planes of movement) In UMN rigidity (clasp knife), why is it resistance found in only some ranges of motion? - Certain sets of muscles are stronger than an

Answer 256

Bradykinesia is another feature of Parkinsonism. It is the poverty (reduction in amount) of movement. How does bradykinesia present across the body? - Hypophonia (soft speech) - Hypomimia (paucity of blinking/ mask-like face) - Arms: Decremental bradykinesia, reduced arm swing when walking, micrographia - Legs: Smaller stride and festinant/ Parkinsonian gait Stride and gait abnormalities would mak

Answer 257

"Outline the causes of Parkinsonism - Idiopathic Parkinson Disease - Neuroleptic Medication - Wilson Disease - Parkinson plus syndromes - Infective encephalitis - Vascular Parkinsonism (Multi-infarct dementia from malignant HTN) But the presentation of this syndrome doesn't mean the patient definitely has Parkinson disease. Therefore we have to exclude the others: Neuroleptic medications (possible

Answer 258

"Outline the causes of Parkinsonism - Idiopathic Parkinson Disease - Neuroleptic Medication - Wilson Disease - Parkinson plus syndromes - Infective encephalitis - Vascular Parkinsonism (Multi-infarct dementia from malignant HTN) But the presentation of this syndrome doesn't mean the patient definitely has Parkinson disease. Therefore we have to exclude the others: Neuroleptic medications (possible

Answer 259

"Outline the causes of Parkinsonism - Idiopathic Parkinson Disease - Neuroleptic Medication - Wilson Disease - Parkinson plus syndromes - Infective encephalitis - Vascular Parkinsonism (Multi-infarct dementia from malignant HTN) But the presentation of this syndrome doesn't mean the patient definitely has Parkinson disease. Therefore we have to exclude the others: Neuroleptic medications (possible

Answer 260

Outline the various clinical manifestations of Parkinson's disease (vvvvvv IMPT!!!) Motor symptoms: - Bradykinesia - Hypophonia, Hypomimia, Mask-like expression, Decremental Micrographia, Festinant Gait/ Parkinsonian Gait, Retropulsion - Resting tremor - Lead-pipe/cogwheel rigidity Non-motor symptoms: - Psychiatric, Depression, Dementia, Mild cognitive impairment - Sleep/fatigue, REM sleep disorde

Answer 261

Outline the various clinical manifestations of Parkinson's disease (vvvvvv IMPT!!!) Motor symptoms: - Bradykinesia - Hypophonia, Hypomimia, Mask-like expression, Decremental Micrographia, Festinant Gait/ Parkinsonian Gait, Retropulsion - Resting tremor - Lead-pipe/cogwheel rigidity Non-motor symptoms: - Psychiatric, Depression, Dementia, Mild cognitive impairment - Sleep/fatigue, REM sleep disorde

Answer 262

"Treatment for Parkinson's Disease (vvvvvvvvvvv IMPT!!) What does treatment of Parkinson's Disease aim towards? What is the gold standard? re-dressing the dopamine deficit. Gold standard treatment is L-DOPA. But why not just give DOPA? Why got the L infront? Dopamine too large to cross BBB, will hang around in circulation doing everything else except getting into the brain Ok so we give L-DOPA. Bu

Answer 263

"Treatment for Parkinson's Disease (vvvvvvvvvvv IMPT!!) What does treatment of Parkinson's Disease aim towards? What is the gold standard? re-dressing the dopamine deficit. Gold standard treatment is L-DOPA. But why not just give DOPA? Why got the L infront? Dopamine too large to cross BBB, will hang around in circulation doing everything else except getting into the brain Ok so we give L-DOPA. Bu

Answer 264

"Treatment for Parkinson's Disease (vvvvvvvvvvv IMPT!!) What does treatment of Parkinson's Disease aim towards? What is the gold standard? re-dressing the dopamine deficit. Gold standard treatment is L-DOPA. But why not just give DOPA? Why got the L infront? Dopamine too large to cross BBB, will hang around in circulation doing everything else except getting into the brain Ok so we give L-DOPA. Bu

Answer 265

E Resting tremor is typical of parkinsonism Patients typically walk with festinant gait leadpipe/cogwheel ridigity Hypomimia --> paucity of blinking and mask like face

Answer 266

What are the 2 most important Red flags of sinister headaches? (IMPT!!!) - Raised ICP - Neurological deficit Other redflags? (but not seen in all sinister headaches) - tempo (sudden onset or evolving) - constitutional (weight loss/ fever/ confusion and seizures) - elderly (think tumours and temporal arteritis) - meningitic features (fever, headache, photophobia, neck ache etc) In the elderly tempo

Answer 267

What are the 2 most important Red flags of sinister headaches? (IMPT!!!) - Raised ICP - Neurological deficit Other redflags? (but not seen in all sinister headaches) - tempo (sudden onset or evolving) - constitutional (weight loss/ fever/ confusion and seizures) - elderly (think tumours and temporal arteritis) - meningitic features (fever, headache, photophobia, neck ache etc) In the elderly tempo

Answer 268

B Features of raised ICP - Clear postural/pressure features (worse on cough/sneezing/bending over/visual obscurations on bending over) - Worse in night than day - Headache upon waking w vomiting - Pulsatile tinnitus Raised ICP doesnt lead to increased cup-disc ratio (enhanced disc cupping). Thats glaucoma. Raised ICP causes optic disc swelling and oedema (blurred margins), which is collectively ca

Answer 269

Features of raised ICP (IMPT!!!!) - Clear postural/pressure features (worse on cough/sneezing/bending over/visual obscurations on bending over) - Worse in night than day - Headache upon waking w vomiting - Pulsatile tinnitus Pt 1, anything that strains the body would cause pain. Visual obstructions when bending over is a serious sign because it means that ICP is high enough to drop perfusion press

Answer 270

What is the diff between raised ICP and glaucoma? Raised ICP impedes venous flow from back of eye --> optic disc swelling and oedema (blurred margins), which is collectively called papilloedema Glaucoma pressure is inside the eye --> no disc swelling, only enhanced disc cupping which 3 cranial nerves are vulnerable to raised ICP? Why? CN VI (most vulnerable) as it emerges from the lip of foramen m

Answer 271

What is a reflex arc made of? Afferent limb (sensory neuron) + efferent limb (LMN) What are the physiological functions of the reflex arc? - Prevents overstretching of muscle - protective - Helps maintain posture - Generates tone UMN input modulates and regulates reflex.

Answer 272

What is a reflex arc made of? Afferent limb (sensory neuron) + efferent limb (LMN) What are the physiological functions of the reflex arc? - Prevents overstretching of muscle - protective - Helps maintain posture - Generates tone UMN input modulates and regulates reflex.

Answer 273

What is a reflex arc made of? Afferent limb (sensory neuron) + efferent limb (LMN) What are the physiological functions of the reflex arc? - Prevents overstretching of muscle - protective - Helps maintain posture - Generates tone UMN input modulates and regulates reflex.

Answer 274

What presentations would suggest CNS lesion? (vvvvv IMPT!!!) - UMN lesions - Cerebellar/ Basal gangia (nuclei symptoms) eg ataxia - Cognitive signs - Visual field defects (all visual field defects are CNS problems eg hemianopia) What presentations would suggest PNS lesion? (vvvvv IMPT!!!) - Exclusively LMN issues - Muscle/ NMJ issues (eg Myasthenia Gravis, peripheral neuropathies) LMN mostly PNS e

Answer 275

What presentations would suggest CNS lesion? (vvvvv IMPT!!!) - UMN lesions - Cerebellar/ Basal gangia (nuclei symptoms) eg ataxia - Cognitive signs - Visual field defects (all visual field defects are CNS problems eg hemianopia) What presentations would suggest PNS lesion? (vvvvv IMPT!!!) - Exclusively LMN issues - Muscle/ NMJ issues (eg Myasthenia Gravis, peripheral neuropathies) LMN mostly PNS e

Answer 276

UMN “CNS” pattern weakness presents with? (vvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvv IMPT!!!) - Hyperreflexia - Hypertonia (clasp-knife) - Spasticity - Other signs like pronator drift (yes it's an UMN sign) LMN “PNS” pattern weakness presents with? (vvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvv IMPT!!!) - Areflexia - Hypotonia - Muscle wasting - Fasciculations For understanding: In UMN lesions, high

Answer 277

If you get both signs of hyperreflexia (UMN lesion) AND fasciculation (LMN lesion) at different area of the body, where is the lesion? Prob CNS, at spinal cord This is because you can have lesions at the spinal segments, obliterating LMN at that segmental level and obliterating UMN at levels below that. See pic! At the level where there is lesion to LMN, LMN signs would dominate because the end co

Answer 278

Summary of lesions (IMPT!!!) Brain: Cerebrum: UMN, Contralateral Brainstem: UMN, Contralateral (+/- ipsilateral face because of CN VII double innervation) Cerebellum: Pure ataxia, Ipsilateral Cord: Cervical: UMN, sphincteric involvement, sensory level, LMN Thoracic: UMN, sphincteric involvement, sensory level, LMN LS: UMN, sphincteric involvement, sensory level, LMN

Answer 279

Summary of lesions (IMPT!!!) Brain: Cerebrum: UMN, Contralateral Brainstem: UMN, Contralateral (+/- ipsilateral face because of CN VII double innervation) Cerebellum: Pure ataxia, Ipsilateral Cord: Cervical: UMN, sphincteric involvement, sensory level, LMN Thoracic: UMN, sphincteric involvement, sensory level, LMN LS: UMN, sphincteric involvement, sensory level, LMN

Answer 280

Dorsal Column Medial Lemniscus (DCML) and corticospinal (lateral tract) fibres decussate at lower brainstem Spinothalamic Fibres decussate at level of entry This one if dk then really honggan!! MEMORIZE!! DCML and cortical spinal (lateral tract) decussate at lower brainstem spinothalamic decussate at level of lower brainstem Spinothalamic is pain and temperature (lateral) + crude touch and pressur

Answer 281

"name some cerebral hemisphere lesions signs (vvvvvv IMPT!!!) - Hemiparesis - Visual field defects - Cognitive deficits - dysphasia (higher cognitive function) - dyscalculia (higher cognitive function) - agnosia (higher cognitive function) - neglect (higher cognitive function) Impt concept - Subcortical lesions (white matter) tend to give rise to pure motor/sensory syndromes - Cortical lesions (gr

Answer 282

Brain has large cross section, hence lesion likely to affect only 1 side (unilateral signs) Cord has small cross section, hence lesion likely to affect both sides (bilateral signs) and sphincteric involvement (urological symptoms)

Answer 283

For brain lesions, what are the signs that points towards a lesion in the Cerebral hemispheres? - Hemiparesis - +/- visual defect - +/- cognitive defects - +/- Higher cognitive defects (dysphasia, dyscalculia, agnosia, neglect) Brainstem? - CN signs (home of the CNs) - Ataxia/vertigo - Double vision Cerebellum - Pure ataxia

Answer 284

For brain lesions, what are the signs that points towards a lesion in the Cerebral hemispheres? - Hemiparesis - +/- visual defect - +/- cognitive defects - +/- Higher cognitive defects (dysphasia, dyscalculia, agnosia, neglect) Brainstem? - CN signs (home of the CNs) - Ataxia/vertigo - Double vision Cerebellum - Pure ataxia

Answer 285

Summary of presentations of PNS lesions. Think root, plexus, nerve, NMJ, Muscle. Then think pattern, distribution and comments.

Answer 286

Why are reflexes still present in muscle or NMJ lesions? Lesions here tend to be partial and cause partial weakness. Therefore there will still be a reflex until the weakness is super profound. So in diseases such as polymyositis and Guillain-Barre, reflexes would still remain.

Answer 287

Lumbosacral plexus injury tends to be at level of L4-S1 Can mimic sciatic nerve injuries (same roots) Eh slides say this is impt eh:

Answer 288

median nerve kena whack = Carpel Tunnel Syndrome Radial nerve kena whack = Saturday Night Palsy Ulnar nerve kena whack = Cubital tunnel syndrome Just read the slides.

Answer 289

General observations about LMN (roots, plexus and nerve) Are part of LMN, so will have areflexia, hypotonia, wasting, fasciculations, weakness, sensory abnormalities General observation about nerves Long nerves more vulnerable to systemic insults than short nerves. Henceit affects the extremities of limbs first (glove and stocking distribution weakness and numbness) (all 4 limbs, but usually feet

Answer 290

General observations about LMN (roots, plexus and nerve) Are part of LMN, so will have areflexia, hypotonia, wasting, fasciculations, weakness, sensory abnormalities General observation about nerves Long nerves more vulnerable to systemic insults than short nerves. Henceit affects the extremities of limbs first (glove and stocking distribution weakness and numbness) (all 4 limbs, but usually feet

Answer 291

NMJ and Muscle lesions What are signs of proximal myopathy (muscle lesions)? - Proximal weakness - Wasting without fasciculations - +/- Pseudohypertrophy What are signs of NMJ lesions? - Proximal weakness - Ocular weakness - Fatiguability Why does NMJ and muscle lesions both present with proximal weakness? Why not distal? Proximal muscles exert much more force than distal muscles. So when muscles

Answer 292

NMJ and Muscle lesions What are signs of proximal myopathy (muscle lesions)? - Proximal weakness - Wasting without fasciculations - +/- Pseudohypertrophy What are signs of NMJ lesions? - Proximal weakness - Ocular weakness - Fatiguability Why does NMJ and muscle lesions both present with proximal weakness? Why not distal? Proximal muscles exert much more force than distal muscles. So when muscles

Answer 293

NMJ and Muscle lesions What are signs of proximal myopathy (muscle lesions)? - Proximal weakness - Wasting without fasciculations - +/- Pseudohypertrophy What are signs of NMJ lesions? - Proximal weakness - Ocular weakness - Fatiguability Why does NMJ and muscle lesions both present with proximal weakness? Why not distal? Proximal muscles exert much more force than distal muscles. So when muscles

Answer 294

Hemineglect, also known as unilateral neglect, hemispatial neglect or spatial neglect, is a common and disabling condition following brain damage in which patients fail to be aware of items to one side of space. Which part of the brain is affected in hemineglect? contralateral parietal lobe

Answer 295

On CT, Cerebral ischemia is hypodense (dark) Cerebral haemorrhage is hyperdense (bright)

Answer 296

"What are the investigations for (IMPT!!!) Syncope? - normally not investigated in young (hyperattenuated vagal systems) unless recurrent - then look for cardiac issues (ECG & 24hr holter monitoring) - and autonomic features (tilt table) Seizures? - Look for electrolyte abnormalities (renal panel) and infective precipitants (FBC, culture) - :then look for electrical abnormalities in the brain (EEG

Prof Derrik soon Anki Flashcards

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