Neurology Flashcards

Question

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Answer 1

Inflammation of the leptomeningeal (pia mater and arachnoid) coverings of the brain, most commonly caused by infection.

Answer 2

BACTERIAL: Babies <3 months: Group B streptococcus, E Coli, L monocytogenes Children and babies >3 months: N meningitidis, S pneumoniae, H influenzae (now rare due to vaccine). Adults: N meningitidis, S pneumoniae, TB Elderly: S pneumoniae, L monocytogenes *Staph Aureus with Hx of neurosurgical procedures of trauma to the head Other, less common but important bacterial causes: - Mycobacterium tuberculosis (Hx of exposure to TB, e.g. infants in endemic areas) - Lyme meningitis (spirochete Borrelia burgdorferi, Hx travel to endemic region) - Rock mountain spotted fever (Rickeettsia reicketsii, carried by dog tick, endemic to central & south america) - Neurosyphilis (rare in sexually active individuals esp immunocompromised ones) ASEPTIC: VIRAL: Enteroviruses (Coxsackie or Echovirus) are most commmon cause of viral meningitis, mumps, HSV, VZV, HIV. FUNGAL: Cryptococcus (associated with HIV infection). PARASITES: Naegleria fowleri: "brain eating amoeba) OTHERS: Aseptic meningitis, Mollaret’s meningitis ``` RISK FACTORS: Close communities (e.g. dormitories), basal skull fractures, mastoiditis, sinusitis, inner ear infections, alcoholism, immunodeficiency, splenectomy, sickle cell anaemia, CSF shunts, intracranial surgery. ```

Answer 3

Aseptic meningitis : Characterized by clinical and laboratory evidence for meningeal inﬂammation and negative routine bacterial cultures Most common cause entrovirus

Answer 4

TRIAD: Fever, headache, , neck rigidity, Other common: photophobia, irritability, drowsiness, vomiting, high-pitched crying or fits. clouding of consciousness. Time course: Acute bacterial meningitis & HSV meningoencephalitis- Hrs to few days Viral meningitis, cryptococcal meningitis : days to weeks TB, sypholis: over months

Answer 5

Signs of meningism: Photophobia, neck stiffness (Kernig's sign: with hips flexed, pain/resistance on passive knee extension; Brudzinski 's sign: flexion of hips on neck flexion). Signs of infection: Fever, tachycardia and hypotension, skin rash (petechiae with meningococcal septicaemia), altered mental state.

Answer 6

Blood: 2 sets of blood cultures (do not delay Abx) Imaging: CT scan to exclude mass lesion/raised ICP before doing an LP (or it may lead to cerebral herniation during subsequent CSF removal)/ CT head must be done before LP in patients with: immunodeficiency, history of CNS disease, reduced consciousness, fit, focal neuro deficit or papilloedema LP: Note opening CSF pressure. Send CSF for microscopy with, culture, sensitivity and Gram staining ( Streptococcus pneumoniae : Gram-positive diplococcic, Neisseria Meningitidis : gram-negative diplococcic), biochemistry and cytology. Bacterial infection on LP: cloudy CSF, WBCs in 1000s with neutrophil pleocytosis (>80%), protein, reduced glucose (CSF: serum glucose ration of <0/5) Viral infection on LP: WBCs in 100s with lymphocytic pleocytosis (>50%), protein but NORMAL glucose Note that in fungal and TB meningitis, WBCs in 100s but there is mononuclear pleocytosis (>50%) TB: Fibrinous CSF, increased lymphocytes. raised protein and reduced glucose Staining of petechiae scrapings may detect meningococcus in ~70%. Additional studies e.g. viral PCR, staining/culture for mycobacteria and fungi, HIV test depending on the clinical presentation/CSF findings.

Answer 7

ABx: Immediate IV/IM antibiotics if meningitis suspected (before lumbar puncture or CT). Third-generation cephalosporin are given because they can cross the BBB! (cefotaxime 2 g qds or ceftriaxone 2 g bd). The reason is that Benzylpenicillin may be given as initial blind therapy and for sensitive meningococci and pneumococi. Amoxicillin þ gentamicin for Listeria . For penicillin and cephalosporin resistant pneumococci: add vancomycin and if necessary rifampicin. If there is history of anaphylaxis to penicillin or cephalosporins or if the organism is resistant to these, use chloramphenicol. Give rifampicin for 2 days to patients treated with benzylpenicillin or chloramphenicol (to eliminate nasopharyngeal carriage). DEXAMETHASONE: IV (10 mg QDS for 4 days) given shortly before or with first dose of antibiotics. Continue in pneumococcal or H. influenzae meningitis: reduced complications: death ( S. pneumoniae ) and hearing loss ( H. influenza ). Avoid dexamethasone if HIV is suspected. RESUSCITATION: best managed in ITU PREVENTION: (only applicable to meningococcal meningitis): Notify public health services and consult a consultant in communicable disease control for advice regarding chemoprophylaxis (e.g. rifampicin for 2 days) and vaccination for close contacts. Vaccination against meningococcal serogroups A and C. (Note that there is no vaccine for serogroup B, the most common serological group

Answer 8

Sensorineural deafness is most common Subdural effusions occur secondary to Haemophilus influenzae meningitis and may progress to a subdural empyema. .Septicaemia, shock, DIC, renal failure, fits, peripheral gangrene, cerebral oedema, cranial nerve lesions, cerebral venous thrombosis, hydrocephalus, Waterhouse– Friderichsen syndrome (bilateral adrenal haemorrhage).

Answer 9

Mortality rate from bacterial meningitis is high (10– 40% with meningococcal sepsis). In developing countries mortality rate often higher. Viral meningitis self-limiting.

Answer 10

This is when the meningitis is caused by either viruses, mycobacteria (e.g. TB), fungi or parasites Because routine bacterial cultures of the CSF will be -ve in these cases. Note that bacterial meningitis is NOT aseptic

Answer 11

Abnormal brain function in pure encephalitis but not meningitis Meningeal irritation symptoms (such as neck rigidity) in meningitis but not pure encephalitis Seizures in both. Note that meningeal irritation symptoms may occur in meningoencephalitis

Answer 12

Neisseria meningitidis

Answer 13

Rock mountain spotted fever

Answer 14

Lyme disease meningitis

Answer 15

West nile virus

Answer 16

If they also had pulmonary infiltrates, lymphadenopathy and a +ve tuberculin skin test

Answer 17

If individual has features of encephalitis: abnornal brain function, fussiness or lethargy in infants, temporal lobe enhancement on CT Crucial to NOT DELAY acyclovir if HSV enceph is a possibility

Answer 18

The brainstem

Answer 19

Bacterial 100-500 Viral 15-200 Fungal 15-200 TB 100-500 Bacteria and TB cause higher levels of protein in the CSF because they cause more inflammation, which increases the permeability of the BBB more than the other causes of meningitis, allowing more protein in

Answer 20

In bacterial/fungi the glucose will be reduced, but in viral it will be normal This is because bacterial/fungal inflammation causes less gluocse to enter through the BBB as it blocks the glucose transporters

Answer 21

TB PCR preferred because it is more sensitive and faster Looking for AFB on microscope takes weeks and is low yield

Answer 22

India ink stain showing broad budding yeast and a thick fungal capsule that does not take up the stain The cryptococcal capsular antigen test is more sensitive and more commonly used

Answer 23

Small spherules on microscopic examination but serum serology is now mainstay

Answer 24

Presence of RBCs

Answer 25

Weakness or paralysis of the muscles on one side of the face, caused by damage to the seventh cranial nerve, which is the facial nerve The seventh cranial nerve, the facial nerve, emerges from the brainstem, and then enters the temporal bone where it travels through a narrow, Z-shaped canal, called the facial canal. The facial nerve exits the skull through a tiny hole called the stylomastoid foramen. - Innervates facial muscles - Innervates the sublingual and submandibular glands, which secrete saliva, the lacrimal gland which produces tears, and mucous membranes of the nose, mouth, and nasopharynx. - it innervates the stapedius muscle which dampens the vibration of the stapes, a small bone that help transmit vibrations from the eardrum; this protects you from loud noises. - carries sensory information about taste from the anterior ⅔ of the tongue.

Answer 26

The underlying cause of cranial nerve damage is idiopathic which means it’s unknown, so when there’s facial nerve a paralysis from a known cause like a stroke, a tumor, or trauma, it’s not considered a Bell’s palsy. Bell’s palsy occurs when the facial nerve gets damaged, and although the precise cause is unknown, it’s often associated with viral infections like: - herpes simplex virus, - Epstein-Barr virus, and varicella-zoster virus - the bacteria Borrelia burgdorferi which causes lyme disease. RISK FACTORS: Age (peak incidence > 50), diabetes mellitus, pregnancy (third trimester), early postpartum

Answer 27

Unilateral facial weakness (evolves rapidly over 48hr) Absence of nasolabial fold Drooping of eyelid Drooping of mouth Dryness of affected eye/mouth Hypersensitivity to loud noises (hyperacusis) Loss of taste sensation on anterior 2/3 of tongue (ageusia) (relate all of these to the function of the facial nerve)

Answer 28

Unilateral facial weakness (evolves rapidly over 48hr) Absence of nasolabial fold Drooping of eyelid Drooping of mouth Dryness of affected eye/mouth Hypersensitivity to loud noises (hyperacusis) Loss of taste sensation on anterior 2/3 of tongue (ageusia) (relate all of these to the function of the facial nerve) ``` Mnemonic: Blink reflex abnormal Ear sensitivity Lacrimation: deficient, excess Loss of taste, Sudden onset Palsy: CN VII nerve muscles (all symptoms unilateral) ```

Answer 29

Lab: serological testing if viral infection suspected Motor nerve conduction studies can be performed if there is no recovery after a few weeks to assess for the presence of axonal degeneration Others: House-brackmann facial nerve dysfunction classification Palpebral-oculogyric reflex (Bell phenomenon): attempted eyelid closure -->upward eye deviation Reduced pinprick sensation in posterior auricular area Reduced taste The diagnosis of a Bell’s palsy is based on identifying that the problem is with the facial nerve and not finding an alternative explanation like a stroke or brain tumor.

Answer 30

Treatment isn’t needed in all cases of Bell’s palsy, but in some severe cases, corticosteroids can help reduce the nerve inflammation and speed up the recovery. In most cases, symptoms usually subside on their own Other: artifical tears, eye patching (reduce corneal damage risk), physical therapy (facial exercise, NM retraining)

Answer 31

Permanent facial weakness or paralysis You might get severe ectropian requiring partial lidsuturing

Answer 32

Most people recover within 6 months after the onset, but some people develop permanent facial weakness or paralysis. Most patients with partial paralysis recover completely and rapidly, although in those with complete paralysis recovery may not occur until after 3 months. Recovery may be incomplete and in some patients with axonal degeneration abnormal reconnections may occur e.g. production of tears on eating. Surgery should not be considered until time for recovery (> 3 months) has been allowed.

Answer 33

The lower motor neurons innervating the bottom half of the face receive innervation from upper motor neurons originating on the contralateral side The lower motor neurons innervating the top half of the face receive innervation from upper motor neurons originating on both the ipsilateral and the contralateral side (i.e. they have dual innervation) Thus, in a stroke (affecting the upper motor neurons), the top half of the face will be spared, because the stroke will only affect one side of the brain, but the lower motor neurons for the top half of the face receive dual innervation, so they will still receive innervation from the upper motor neuron not affected by the stroke HOWEVER, In Bell's palsy, there is a disease of the LOWER motor neuron so although both the ipsilateral and contralateral supply to the lower motor neuron is fine, the damage to the lower motor neuron itself means that the muscles in the top half of the face will be paralysed

Answer 34

Autoimmune condition where inflammatory plaques of demyelination in the cns disseminated in space and time; ie occuring at multiple sites, with ≥30d in between attacks Demyelination heals poorly, eventually causing axonal loss; >80% of patients develop progressive disability. 1. Relapsing, remitting (commonest. Complete recovery in between attacks) 2. Clinically isolated syndrome (single clinical attack of demyelination. Not actually MS, but 10-15% develop it after) 3. Primary progressive MS (steadily accumulation of disability with no relapsing-remitting pattern) 4. Secondary progressive: Symptoms worsen more steadily over time, with or without the occurrence of relapses and remissions. Most people who are diagnosed with relapsing-remitting multiple sclerosis will transition to SPMS at some point (due to poor axonal healing) 4. Marburg variant (severe filminant variant of MS leading to advanced disability or death within a period of weeks)

Answer 35

The exact cause of the disease remains unknown; it is most likely a combination of genetic and environmental factors. Immune-mediated damage to CNS myelin results in impaired conduction along axons. There is also associated grey matter atrophy. Type IV hypersensitivity reaction! T cells attacking myelin. This then causes antibody reaction to myelin and cell mediated attack of oligodendrocytes. Leaves behind plaques. Risk factors: -Role for EBV exposure and prenatal vitamin D levels have been proposed based on epidemiological studies. - Strong concordance in monozygotic versus dizygotic twins (25% vs 3%). - HLA-DR 2 - Geographical variation (temperate > tropical) with individuals carrying the risk of their pre-pubertal ( < 13 years) country of origin.

Answer 36

Mean age of onset is 30yrs. ♀:♂ ≥3:1. Rare in tropical countries

Answer 37

Depends on site of inflammation 1. Optic neuritis (commonest)- unilatral deterioration in visual acuity and colour perception + PAIN on eye movement 2. Sensory system: Pins and needles, numbness, burning. 3. Motor: Limb weakness, spasms, stiffness, heaviness. 4. Autonomic: Urinary urgency, hesitancy, incontinence, impotence. 5. Psychological: Depression, psychosis. Uhthoff’s phenomenon: Transient increase or recurrence of symptoms due to conduction block precipitated by a rise in body temperature. (body gets overheated from hot weather, exercise, fever, or saunas and hot tubs!)

Answer 38

CLASSICALLY: CHARCOT'S NEUROLOGIC TRIAD: 1) Dysarthria (difficult/unclear speech and swallowing) 2) Nystagmus (involuntary rapid eye movements) + plaques in the eyes 3) Intention tremor (plaques along motor pathways) - Optic neuritis 1 : Impaired visual acuity (most common), loss of coloured vision. On fundoscopy, in active disease, there is a swollen optic nerve head, in chronic disease, there may be optic atrophy. - Visual field testing: Central scotoma (optic nerve affected) or field defects (optic radiations affected). - RAPD: Both pupils contract when light is shone on the unaffected side, both pupils dilate when light is swung to the diseased (eye). - Internuclear opthalmoplegia: when trying to look horizontally, there is a failure of adduction of the contralteral eye, indicating a lesion of the contralateral MLF. https://www.youtube.com/watch?v=NAz_g3FDPjw - Sensory: Paraesthesia (vibration and joint position sense loss more common than pain and temperature). - Motor: UMN signs (e.g. spastic weakness, brisk reflexes). - Cerebellar: Limb ataxia (intention tremor, past-pointing and dysmetria on finger-nose test and heel-shin test), dysdiadochokinesis, ataxic wide-based gait, scanning speech. - Lhermitte’s phenomenon: Electric shock-like sensation in arms and legs precipitated by neck flexion.

Answer 39

Diagnosis based on two or more CNS lesions with corresponding symptoms, separated in time and space (McDonald criteria). FIRST INVESTIGATION: MRI-brain, cervical and thoracic spine (with gadolinium contrast): Plaque detection is highlighted as high-signal lesions -"white matter plaques". This can monitor disease progression and help diagnosis Lumbar puncture: Microscopy to exclude other infective or inflammatory causes. CSF electrophoresis shows unmatched oligoclonal bands. Their presence suggests inflammation of the central nervous system due to infection or another disease. If similar bands aren't present in your blood, you may have multiple sclerosis (MS). Evoked potentials: Visual, auditory or somatosensory evoked potentials (VEP, BEP, SEP) may show delayed conduction velocity. VEPs are delayed in ~90% of patients with MS. Visual evoked potentials are used to investigate patients with no clinically obvious or acute optic neuritis who are suspected to have multiple sclerosis (MS), or when there is diagnostic uncertainty about the cause of visual loss. It gives an objective measure of visual pathway function.

Answer 40

Post-ictal neurologic dysfunction (i.e. dysfunction in the altered stage of consciousness following a seizure) Affects same area of brain from which seizure originated ranging from motor, sensory or special sense dysfunction including speech, hearing and vision. Todd's paralysis usually affects the same areas in which the seizure originated. It can also affect speech, gaze, and vision. It can later go through secondary generalisation (i.e. spread to rest of body). Self-limited condition but can require work up for other causes of paralysis e.g. stroke

Answer 41

Conversion disorder describes a condition of neurologic dysfunction with no identifiable organic cause.

Answer 42

Malingering is the deliberate feigning of symptoms to achieve secondary gain, such as a patient faking abdominal pain to receive a prescription for narcotic pain medications. Patients who act paralyzed often display give-away weakness. This includes maintenance of strength for a brief period followed by voluntary muscle relaxation.

Answer 43

Convulsive (i.e. includes marker motor symptoms e.g. tonic clonic movements) >5mins. If non-convulsive, lasting >10 mins

Answer 44

Anterior cerebral artery injury affects the sensory and motor cortices of the lower extremity, and results in contralateral paralysis and sensory loss of that limb only. It would not affect the face or upper extremity. Behavioural changes Middle cerebral artery - affects the sensory and motor cortices of the face> upper extremity> leg - Broca area, and Wernicke area so problems with speech fluency/language comprehension problem - loss of contralateral half of visual field PCA strokes like diplopia, visual field defects, dysphagia, vertigo, alteration in consciousness, memory impairment, or difficulty reading

Answer 45

F... Comprehension is mildly to moderately impaired in expressive aphasia.

Answer 46

Global aphasia is a severe impairment of both expressive and receptive skills. It is caused by a large left hemisphere lesion. People are often alert and are able to express themselves through facial expressions, intonation, and gestures. Anomic aphasia is a mild form of aphasia. The most prominent difficulty is in word-finding, with the person using generic fillers in utterances, such as nonspecific nouns and pronouns, or circumlocution, where the person describes the intended word. Comprehension and repetition of words, and sentences is typically good. Conductive aphasia is characterized by prominent impairment with repetition. Damage typically involves the arcuate fasciculus and the left parietal region. The patient is able to express him- or herself fairly well, with some word-finding issues, and comprehension can be functional.

Answer 47

Knowledge of this syndrome relies on the neuroanatomic knowledge of the cross-sectional spinal cord tract pathways: 1. pain/temperature via spinothalamic tract, 2. motor via corticospinal tracts, and 3. tactile/vibration sensation via dorsal column medial lemniscus (DCML) tracts. ACS leads to ischemia of the former two anteriorly located tracts, with preservation of the DCML tract, as supplied by the posterior spinal artery. Presents with bilateral motor and temperature/pain sensory deficits, with intact pinpoint and vibratory sensation due to the preserved dorsal DCML pathways.

Answer 48

Whereas B12 deficiency will have loss of proprioception, folate deficiency will not have any neurologic dysfunction. This is because Vitamin B12 deficiency can lead to an accumulation of methylmalonic acid which causes dysfunction of the dorsal columns and lateral corticospinal tract. This relatively rare symptom is known as subacute combined degeneration. These patients will have ataxia and loss of proprioception. Note that b12 deficiency will also lead to macrocytic and megaloblasic anaemia

Answer 49

Neurodegenerative disease of the dopaminergic neurones of the substantia nigra (which project to the striatum), characterized by bradykinesia, rigidity, tremor and postural instability (a late symptom).

Answer 50

Pathophysiology: -Degeneration of midbrain dopaminergic neurones projecting from the substantia nigra to the striatum (caudate nucleus and putamen). Surviving neurones often contain eosinophilic cytoplasmic inclusions called Lewy bodies (Lewy bodies are eosinophilic, made of alpha synuclein proteins). Patients only symptomatic after > 70% neuronal loss. Nigrostriatal dopaminergic deficiency causes abnormalities of plasticity in the basal ganglia and cerebral cortex. 1) Sporadic and idiopathic (most common) : Unknown. Environmental toxins and oxidative stress have been proposed (e.g. pesticides, wood pulp). 2) Familial forms : - Genes mutations that cause Parkinson's Disease are in LRRK2, PARK2 (Parkin), PARK7, PINK1 and SNCA ( a -synuclein) genes. PINK1, PARKIN, ALPHA SYNUCLEIN genes 3) IN RARE CASES: A toxic impurity cound in recreational drugs (especially MPPP). The impurity is called MPTP Risk factors: Pesticide exposure Gene variants LRRK2

Answer 51

.Very common: 1– 2% of > 60-year-olds. Annual incidence is 20 in 100000. Mean age of onset is ~ 57 years.

Answer 52

HISTORY: Insidious onset. Tremor AT REST, usually noticed in hands (most present with unilateral UL tremor, this later spreads to involve other limbs). (an intention or action tremor is seen in Benign Essential Tremor, so ensure you distinguish this from Parkinson's) Stiffness and slowness of movements Difficulty initiating movements Frequent falls Smaller handwriting (micrographia) Insomnia, mental slowness (bradyphenia) NARROW gait

Answer 53

Pill rolling tremor at rest Lead pipe rigidity of muscle tone with superimposed tremor (cogwheel rigidity), which can be enhanced by distraction (asking them to raise and lower other arm) Gait: stooped, simian, shuffling, small-stepped fait with reduced arm swing. Freezing (difficulty initiating walking) Postural instability: falls easilty with little pressure from back (propulsion) or front (retropulsion) Others: - Frontalis overactivation (furrowing of brow) - Hypomimia (expressionless face) - Soft monotonous voice (hypophonia) - Impaired olfaction - Mild impairment of up-gaze and tendency to drool - Involuntary movements in one part of the face associated with voluntary movement in another part of the face (synkinesis) Psych: depression common. Cognitive problems and dementia in late disease

Answer 54

Clinical diagnosis: - Levadopa trial and clinical assessment after levodopa - Blood: Serum ceruloplasmin excludes WILSON'S disease in young onset - CT/MRI brain to exclude other causes of gait decline e.g. hydrocephalus, vascular disease - Dopamine transporter scintigraphy (DAT scan): reduction in striatum and putamen. May be necessary for distinguishing from essential tremor.

Answer 55

2- one on each side of the midbrain

Answer 56

This is the one affected in parkinson's. They go from the substantia nigra, which is in the basal ganglia, up to the striatum (=caudate + putamen) in the motor cortex

Answer 57

pars compacta

Answer 58

There is a tremor present at rest which DIMINISHES with movement

Answer 59

NO!!!!! This helps differentiate it from other diseases

Answer 60

Because cerebellar disease have action (=intention) tremor, which is the opposite of the resting tremor seen in parkinson's

Answer 61

In essential tremor there is no bradykinesia, or postural instability Note that in Parkinson's there is NO WEAKNESS.

Answer 62

Idiopathic Parkinson's disease Side effects of medication: - Antipsychotics (haloperidol, blocking dopamine receptors) - Metaclopramide (dopamine antagonist) Rarely: trauma/boxing, encephalopathy post flu, manganese/copper toxicity, HIV, parkinson's plus syndromes Parkinson's plus syndromes: Lewy body dementia Wilson disease Pick disease (a type of fronto-temporal dementia

Answer 63

VIVID V- vertical gaze palsy and early postural instability (this is usually a late feature if it's PD)--> progressive supranuclear palsy I- Impotence/incontinence --> multiple system atrophy V- Visual hallucinations and early dementia--> lewy body dementia I-Autonomous interfering activity by affected limb--> corticobasal degeneration D-diabetic/hypertensive patient with pyramidal signs (leg) and falls, ataxia --> vascular parkinsonism

Answer 64

``` Loss of smell Depression and dementia Visual hallucinations Dribbling of saliva Constipation ```

Answer 65

Enlargement of the ventricular system in the brain caused by impaired drainage of cerebro-spinal fluid

Answer 66

Divisible into obstructive and npn-obstructive (communicating and non-communicating) Communicating= impaired outflow of the CSF from the ventricular system: 1. Lesions of 3rd, 4th ventricle or aqueduct 2. Posterior fossa lesions compressing 4th ventricle (e.g tumour blood) 3. Cerebral aqueduct stenosis Non communicating= impaired CSF resorption in the subarachnoid villi: 1. Tumours 2. Meningitis (typically TB) 3. Normal pressure hydrocephalus (see below)

Answer 67

Bimodal age distribution. Congenital malformations and tumours in the young, tumours and strokes in the elderly.

Answer 68

Obstructive hydrocephalus : Headaches. Vomiting. Seizures. Acute drop in conscious level. Balance problems. Diplopia. NPH : Chronic cognitive decline, falls, urinary incontinence.

Answer 69

Obstructive hydrocephalus : Impaired GCS, papilloedema, VI nerve palsy ("false localizing" sign of increased ICP). In neonates, the head circumference may enlarge, and "sunset sign" (downward conjugate deviation of eyes). In children, enlarged head, developmental delay, intellectual disability, muscle spasticity NPH : Cognitive impairment. Gait apraxia (shuffling). Hyper-reflexia.

Answer 70

CT head : First-line investigation to detect hydrocephalus. May also detect the cause (e.g. tumour in the brainstem). CSF : Obtained from ventricular drains or lumbar puncture may indicate an underlying pathology (e.g. tuberculosis). Check for MC&S, protein, glucose (CSF and plasma). The best way to diagnose aqueduct stenosis is with an MRI because it can visualise the entire length of the aqueduct Lumbar puncture : This is contra-indicated in obstructive hydrocephalus as it can cause tonsilar herniation and death. May be necessary in NPH as a therapeutic trial.

Answer 71

Term used to describe apparent enlargement of ventricles but this is a compensatory change due to brain atrophy

Answer 72

A type of non communicating hydrocephalus. Idiopathic chronic ventricular enlargement. The long white matter tracts (corona radiata, anterior commisure) are damaged causing gait and cognitive decline.

Answer 73

Manage emergencies with ABC, and manage seizures Surgical insertion of a ventriculoperitoneal shunt. Helps to reduce ICP. Implantation of a ventricular catheter into one or both lateral ventricles and connecting it to a subcutaneous drain which leads to the peritoneal cavity. Carries risk of shunt infection, block or malfunction (especially as some are electronic). Lumbar-peritoneal shunting : Alternative procedure that may be suitable for communicating hydrocephalus. Advanced neurosurgery : Endoscopic ventriculostomy and aqueductoplasty are other options used to bypass blockages or maintain patency for CSF flow. Also physiotherapy to help develop motor skills

Answer 74

Chronic neurological condition with recurrent seizures >2 seizures REQUIRED for diagnosis Partial (=focal): - One hemisphere affected. - More likely to be due to a structural abnormality - Preceded by aura e. g. Frontal lobe focal motor seizure, temporal lobe seizures, frontal lobe complex partial seizures Partial seizures are usually "simple" (i.e. awareness not impaired, no post-ictal symptoms, auras present), but can also be "complex" (i.e. awareness impaired, post-ictal confusion common, may have auras). Can also undergo secondary generalisation. Generalised: - Both hemispheres - LOC occurs - More likely idiopathic/congenital e. g. Tonic, clonic, tonic-clonic, atonic, myoclonic, absence,

Answer 75

Classify into provoked (acute symptomatic) seizures (INVITED MD), and unprovoked seizures (which can occur due to a genetic problem, or a metabolic/structural abnormality) - Family Hx - Febrile convulsions - Autism/ADHA - Cerebral palsy/stroke CAUSES: Idiopathic- 2/3 Infection: meningitis/encephalitis/abscess (including scarring from previously having these infections) Neoplasm: Tumour Vascular: stroke, haemorrhage, malignant hypertension or eclampsia Inflammation: SLE, PAN, rarely MS Toxic/metabolic: sodium imbalance, hyper- or hypoglycaemia, hypocalcaemia, hypoxia, prophyria, liver failure) E- Drugs, including withdrawal from alcohol and benzos) Metabolic above Degenerative: Alzheimer's disease PATHO: Epislepsy results from an imbalance in the inhibitory and excitatory currents (e.g. Na þ or K þ ion channels) or neurotransmission (i.e. glutamate or GABA neurotransmitters) in the brain. Precipitants include any trigger which promotes excitation of the cerebral cortex (e.g. flashing lights, drugs, sleep deprivation, metabolic), but often cryptogenic.

Answer 76

Common. Prevalence in 1% of general population. Peak age of onset is in early childhood or in the elderly.

Answer 77

History: - Rapidity of onset - Duration - Aura (in focal epilepsy) - Tongue biting/loss of continence - Alteration of consciousness - Trigger? Lack of sleep, stress - Did anybody witness - Jerking? - Posticteral state of reduced consciousness? - Drug Hx

Answer 78

Depends on aetiology, usually normal between seizures. Look for focal abnormalities indicative of brain lesions.

Answer 79

Blood: FBC, U&E, LFTs, glucose, Ca 2+ , Mg 2+, prolactin (transient increase shortly after a "true" seizure). ECG CT/MRI: For structural, space-occupying and vascular lesions. EEG (supportive): Helps confirm or refute the diagnosis; assists in classifying the epileptic syndrome. Usually performed inter-ictally and often normal and does not rule out epilepsy. Ictal EEGs combined with video telemetry are more useful but requires adequate facilities. Other investigations: Particularly for secondary seizures according to suspected aetiology e.g. lumbar puncture, HIV serology. , ABG, toxicology screen,

Answer 80

Conservative: - Check time (call ambulance if >5 minutes) - Protect head and loosen tight clothing. - DON'T hold them down, put anything in their mouth, move them unless in danger - Put them in recovery position and minimise their embarrassment (hide incontinence) after Pharmacological: -Basic: carbamazepine/lamotrigine for partial seizures, valproate for generalised Partial seizures (+/- secondary generalisation): - Carbamazepine, lamotrigine (1st line) - Valproate (2nd line) CLV-->VLC Tonic-clonic: - Valproate, lamotrigine (1st line) - Carbamazepine, topiramate (2nd line) Myoclonic, tonic, atonic: Same as tonic-clonic but avoiding carbamazepine Absences: - Valproate, ethosuximide (1st line) - Lamotrigine (2nd line) Contraindications: Carbamazepine: Not to be prescribed if on oral contraceptive pill Valproate: Highly teratogenic, avoid in women of child bearing age Lamotrigine: 1st line for pregnant women

Answer 81

Complications of epilepsy: -Long seizures can lead to hypoxic brain injury Complications of epilepsy management: Antiepileptic drugs, particualry ethosuximide, lamotrigine, carbamezapine, phenytoin, phenobarbital and valproate are notorious for causing skin reactions. Anticonvulsant Hypersensitivity Syndrome occurs in some patients taking anticonvulsant medication. It is characterised by fever, rash, hepatitis and other multiorgan abnormalities. They should not receive should not receive anticonvulsants in the phenytoin category, carbamazepine, phenobarbitone and lamotrigine.

Answer 82

TEMPORAL LOBE FOCAL SEIZURE Most common cause=hippocampal sclerosis Auras: - De ja vu, ja me vu - Olfactory/gustatory hallucination - Auditory hallucinations - Feelings of panic and anger - Memory loss - Dysphasia - Automatisms (lip smacking, chewing, fidgeting etc.)

Answer 83

This is a type of simple partial seizure Frontal lobe focal motor seizure: -Motor convulsions, may demonstrate Jacksonian march (spasm spreading from mouth or digit) followed by post-ictal flaccid weakness (Todd's paralysis)

Answer 84

Loss of consciousness with associated automatisms and rapid recovery.

Answer 85

This a generalised seizure. Vague symptoms before an attack (e.g. irritability), followed by tonic phase (generalised muscle spasm), followed by a clonic phase (repetitive synchronous jerks), and associated faecal or urinary incontinence, tongue biting. After a seizure, there is often impaired consciousness, lethargy, confusion, headache, back pain, stiffness.

Answer 86

Usual onset in childhood. Characterized by loss of consciousness but maintained posture (patient stops talking and stares into space for seconds), blinking or rolling up of eyes with other repetitive motor actions (e.g. chewing). No postictal phase.

Answer 87

Acute confusional state. Often fluctuating. Difficult to distinguish from dementia.

Answer 88

Status epilepticus >30 mins and failure to regain conscioussness (but treatment often initiated in 5-10 mins) : - Secure airway and recovery position - o2 - IV access - IV benzodiazepine: lorazepam (or buccal midazolam/rectal diazepam) given over 2 minutes - Repeat after 15 minutes if necessary - If recur/fail to respond, IV anticonvulsant needed: e.g. phenytoin (15mg/kg) under ECG monitoring. Alternatively, give phenobarbitone, levetiracetam or sodium valproate. - If these fail, consider general anaesthesia, requiring intubation and mechanical ventilcaiton - Treat cause (correct hypoglycaemia or hyponatraemia) - Check plasma levels of all anticonvulsants

Answer 89

Carbamazepine (Na+ channel blocker, extends inactivation)- Hyponatraemia. CI: oral contraceptive pill. Phenytoin (Na+ blocker) : bone mineralisation, gingial hyperplasia Lamotrigine (Na+ channel blocker, selective for excitatory NT like glutatmate)- stevens-johnson syndrome Ethosuximide (Ca2+ channel blocker, thalamic)- sedation Valproate (many: blocks Na, enhance GABA, block Ca) - foetal malormation Topiramate (blocks Na, enhances GABA, blocks NMDA) - cognitive impairment/weight loss kidney stones Levetiracetam (unknown): depression/behavioural/psych issues Carbamazepine, phenytoin, phenobarbitol all p450 inducers Valproate is a p450 inhibitor

Answer 90

This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury. igns and symptoms of SAH include a severe headache with a rapid onset ("thunderclap headache"), vomiting, confusion or a lowered level of consciousness, and sometimes seizures.

Answer 91

You need to do CT-scan first. If this has been ruled negative and there are no clinical signs of increased intracranial pressure, a lumbar puncture is the next step in the work-up. In a CT scan with findings due to SAH, you would see blood pooling in the cisterns. On LP the fluid looks yellow due to xanthochromia (presence of oxidized RBCs)

Answer 92

An arterial bleed into the space between the arachnoid and pia mater of the meninges

Answer 93

85%: burst saccular aneurys in circle of willis 5%: perimesencephalic haemorrhage (parenchymal hammorhage tracking to surface of prain) 5%: AV malformations, bleeding diatheses, vertbral/carotid artery dissection with intracranial extension/mycotic aneurysm/drug abuse (cocaine and amphetamine) ASSOCIATIONS: - HTN, smoking, excess EtOH, SACCULAR ANEURYSMS ASSOCIATED WITH PCKD, marfans, pseudoxanthoma elasticum and Ehlers Danlos syndrome Head trauma

Answer 94

Peak in 5th decade

Answer 95

Sudden onset, thunderclap headache (back of head). Nausea, vomiting, neck stiffness, photophobia Reduced consciousness Subarachnoid hemorrhage (SAH) patients will commonly report having another sudden, severe headache one to three weeks prior. These are known as "sentinel headaches " and are thought to be caused by a minor hemorrhage.

Answer 96

Meningism (blood irritates the meninges): - Neck stiffness, - Photophobia - Kernig's sign Pyrexia Assess GCS Signs of high ICP: - Hypertension with bradycardia - Papilloedema, - Cranial nerve palsy (IV or III) Fundoscopy: Rarely subhyaloid haemorrhage between retina and vitreous membrane Focal neurological signs: -Usually develop on 2nd day, caused by ischaemia from vasospasm and reduced brain perfusion. Aneurysms may cause pressure on cranial nerves causing opthalmoplegia (classically III or VI nerve palsy)

Answer 97

Bloods: FBC, U&E, ESR/CRP, clotting (bleeding diathesis?) Non contrast CT scan: hyperdense areas in the basal regions of the skul caused by blood in the SAH space). Identifies any intraparencymal or intraventricular haemorrhagegs as well LP: increased opening pressure, increased red cells, few white cells, xanthochromia (confirmed by spectrophotometry of CSF supernatant after centrifugation)

Answer 98

An aneurysm of the right carotid artery would cause cavernous sinus syndrome and could produce the symptoms related to compression of CN III, IV, VI, V1 and V2. However, the hormonal changes cannot be attributed to an aneurysm of this blood vessel.

Answer 99

Pseudotumor cerebri is a condition characterized by headaches behind the eye. It is most common in obese women, but typically presents with dizziness, nausea and vomiting. The vision loss associated is usually brief, unlike the long-lasting vision loss experienced by the patient.

Answer 100

Condition by confusion, ataxia and opthalmoplegia

Answer 101

Happens because of the neurological effects of b1 (thiamine) deficiency 1) It is a coenzyme for important enzymes in glucose metabolism 2) In the brain it helps metabolise lipids and carbohydrates and maintain normal AA and neurotransmitter levels 3) In some neurons helps propogate neural impulses down the axon Specifically, thiamine deficiency impairs glucose metabolism and this leads to a decrease in cellular energy. The brain is particularly vulnerable to impaired glucose metabolism since it utilizes so much energy.

Answer 102

Wernicke's encephalopathy is nystagmus, ophthalmoplaegia and ataxia, together with apathy, disorientation and disturbed memory. Treat urgently with thiamine or may progress to Korsakoff 's psychosis. Korsakoff's psychosis is characterized by profound impairment of retrograde and anterograde memory with confabulation, as a result of damage to the mammillary bodies and the hippocampus. Irreversible.

Answer 103

1) First, alcohol interferes with the conversion of thiamine to its active form, thiamine pyrophosphate by blocking the phosphorylation of thiamine. 2) Second, thiamine is normally absorbed through the first portion of the small intestine called the duodenum. However, ethanol prevents this absorption process, and it is believed that alcohol does this by reducing the gene expression for thiamine transporter-1 within the intestinal brush border. 3) Third, chronic alcohol abuse can lead to fatty liver or cirrhosis which interferes with the storage of thiamine within the liver.

Answer 104

Early on in thiamine deficiency, the cerebellum gets affected and that can affect movement and balance. In addition, the brainstem can be affected, and that’s the region that gives rise to the cranial nerves that provide motor and sensory innervation to the face and eyes. If the medulla region of the brainstem is affected, it can impair the heart rate and breathing. Later findings in thiamine deficiency are hemorrhage and necrosis of the mammillary bodies. Wernicke's encephalopathy is characterized by ophthalmoplegia, meaning weakness or paralysis of the eye muscles, ataxia or unsteady gait, and changes in mental state like confusion, apathy, and difficulty concentrating. And untreated Wernicke's encephalopathy can lead to coma and death if not treated quickly. Korsakoff syndrome, on the other hand, mainly targets the limbic system, causing severe memory impairment. One of the characteristic findings of Korsakoff syndrome is confabulation in which the person creates stories to fill in the gaps in their memory which they believe to be true. Not too different from what young children sometimes do in retelling a story.

Answer 105

The therapy is an infusion of thiamine over a few days to get rid of the deficiency. This is then followed by glucose

Answer 106

It’s important to normalize the thiamine levels first, because without thiamine pyrophosphate, most of the glucose will become lactic acid and that can lead to metabolic acidosis.

Answer 107

Lamotrigine

Answer 108

Vasculitides can rarely cause TIA’s hence ESR estimation is useful

Answer 109

This patient needs urgent investigation – usually involving carotid doppler ultrasound and CT/MR of the brain (to look for ischaemia, infarct, bleed, tumour)

Answer 110

F... CT/MR angiography can also be used to non-invasively image the carotid vessels. These techniques are usually used to further evaluate carotid stenoses identified with ultrasound. Conventional angiography is invasive and with risk of stroke is now used less often!

Answer 111

Echocardiogram may also be helpful to assess cardiac function and also can identify mural thrombus/valvular disease/left atrial tumour which can all rarely cause TIA’s. Echo cardiography may also be useful to assess left ventricular function as a marker of end organ damage secondary to hypertension.

Answer 112

Carotid endarterectomy is generally used for patients fit enough to tolerate surgery, who have had a symptomatic TIA/ Stroke with good recovery in the previous 6 months, involving the anterior circulation. Surgery is beneficial in patients with >70% stenosis and surgery itself is not without a small risk of stroke.

Answer 113

Absence of carotid bruit does not exclude a stenosis – indeed a critical stenosis may have almost no flow and bruit will be absent.

Answer 114

Hypoglycaemia, migraine, AF, glioma

Answer 115

Steroids are indicated to reduce cerebral oedema around lesions.

Answer 116

Spirometry

Answer 117

In the context of GBS, the patient is likely to develop type 2 respiratory failure, with pCO2 rising early and pO2 falling later. Thus O2 saturations are not very sensitive. Imaging (CXR and CT chest) may show elevated diaphragms, basal atelectasis and be useful where secondary respiratory compromise through aspiration or PE is suspected.

Answer 118

Both can result in pain in in the temporal region, and be worsened by eating, talking, brushing hair. Loss of vision is exclusive to temporal arteritis In temporal artertitis the pain is constant and severe. Trigeminal neuralgia causes intermittent, sharp pain, often in a mandibular/maxillary distribution. Pain can be worsened by eating, talking but is episodic and severe in nature. It is not associated with visual loss. Trgeminal neuralgia is a symptom of MS!

Answer 119

A lesion of the sympathetic chain causes a Horner’s syndrome with ptosis but does not affect eye movement. 3rd nerve lesion would cause ptosis and affect eye movement Also, the ptosis in 3rd nerve palsy may be complete but in horner's would be very subtle often

Answer 120

F A 3rd nerve lesion can cause COMPLETE ptosis AND a dilated pupil that isn't reactive to light

Answer 121

A rapidly expanding intracranial aneurysm is the most serious cause of an acute third nerve palsy, feared because it can herald rupture of the aneurym. Most common would be microvascular cause (i.e. occlusion of the vasa nervorum of 3rd nerve). This is common in the elderly with HTN In the microvascular (medical cause), the pupil is usually spared (because the parasympathetic supply is on the outside of the nerve, whereas the motor supply is on the inside. The inside of the nerve is affected first by ischaemia (i.e. the motor function including ptosis) before the pupil. In aneurysm cause (surgical cause), then the whole nerve is compressed so pupillary dilation earlier. Other causes include: trauma (12%), compression from neoplasm (11%), postneurosurgery (10%), and compression from aneurysm (6%) and carotid artery dissection

Answer 122

Ischaemic causes (microvascular occlusion in elderly/HTN) are more likely to spare the pupil Compressive causes (rapidly expanding aneurysm) is more likely to involve the pupil early (so is a worrying sign)

Answer 123

F.... A compressive cause (e.g. aneurysm) usually affects the pupil early, is more likely in patients with a family history of intracranial aneurysm, and is more likely to be painful.

Answer 124

Neither CT nor MRI alone are sufficiently sensitive to rule out an aneurysm. Non-invasive angiography (CTA, MRA) is less sensitive for small aneurysms than formal catheter angiography, but is sufficient to rule out a rapidly expanding aneurysm causing a third nerve palsy.

Answer 125

Neglect is due to lesion in parietal lobe | Weakness is due to lesion in frontal lon

Answer 126

F | Lesions in the cerebral hemispheres do not as a rule cause diplopia.

Answer 127

A sudden focal neurological deficit due to cerebrovascular insult. Impairment of CNS function lasts >24hrs. In TIA, it lasts <24hrs.

Answer 128

1) Ischaemic (80%) -Thrombosis: More commonly: In elderly, atherosclerosis usually in smaller cerebral arteries causing lacunar infarcts. Less commonly: atherosclerosis in large vessels e.g. middle cerebral artery. Can arise from prothrombotic states (dehydration/thrombophilia) -Emboli: most commonly cardiac emboli due to AF. Also from carotid artery atheromatous plaques or from intimal flap or carotid dissection). Can get paradoxical embolus from thrombus in the leg slipping through PFO or other atrio-septal defect -Hypoxic: Systemic hypoperfusion/hypoxaemia. Occurs in infants due to iscahemia during birth. Also due to septic shock and drowning - Vasculitis and cocaine 2) Haemorrhagic (20%)- intracerebral (bleeding in brain itself)/subarachnoid haemorrhages (bleeding between pia mater and arachnoid mater) Blood vessel breaks leading to a haematoma which compresses and damages surrounding brain tissue Intracerebral haemorrhage most likely caused by hypertension Subarachnoid haemorrhage most likely caused by ruptured aneursym

Answer 129

Progressively worsen over minutes to hours Depends on location, but symptoms manifest on the contralateral side to the lesion. Anterior cerebral artery: affects feet and legs Middle cerebral artery: hands, arms, face, language centres in dominant hemisphere Posterior cerebral artery: visual cortex Brainstem strokes: both sides ------------------------------------- Modalities affected: Motor. Immediately flaccid paralysis. Then spastic paralysis and hyperreflexia Sensory: numbness & reduced pain and vibration sensation -------------------------------------- Specific types: SAH--> worst headache of life

Answer 130

NIH stroke scale. 11 specific categories, max score 42 - Level of conscioussness - Motor function in arms - Motor function in legs - Visual field tests - Horizontal eye movement - Facial palsy - Limb ataxia - Sensory deficit - Language skills - Speech - Extinction and inattention ----- Check pulse in neck, arms and legs (cardiac cause?) Auscultate for carotid bruits

Answer 131

Check o2 sats and keep above 94% Check glucose level FBC: platelet count, PT, PTT, INR, fibrinogen Cardiac monitor ECG (AF?) --------------------------- Use non contrast CT to distinguish ischaemic and haemorrhagic stroke. (Avoid contrast to avoid mistaking it from blood) *MRI IS ACTUALLY MORE SENSITIVE FOR BOTH HAEMORRHAGIC AND ISCHAEMIC STROKE, BUT CT IS SAFER AND EASIER* You might detect a SAH. Haemorrhagic stroke from HTN will show a homogenous appearing haematoma on CT ------------------------------- SAH can be missed on CT due to small amount of blood, so LP needed can be done to look for RBCs/xanthachromia

Answer 132

Assess ABC. Intubation may be necessary. Hypoxic patients to go on o2. Don't wait for test results unless thrombocytopenia or anticoagulant use is suspected. Ischaemic Thrombolysis with tPA. Ishcaemia is most severe in the core, but slightly less severe in the penumbra. The tPA is focuses on the penumbra -Intravenous tPA if presents within 4.5hrs of symptom onset (or 3hrs of onset for elderly/diabetics). Aspirin NOT given within 24hrs of tPA. IN ADDITION -Mechanical thrombectomy if within 24hrs IF the clot is in the anterior cerebral circulation (ICA, ACA or MCA) OR -Mechanical thrombectomy with stent retriever within 6hrs IF the clot is in the ICA or proximal segment of MCA If present >24hrs after symptom onset, then rectal aspirin immediately Blood pressure control in iscahemic stroke: - There is loss of autoregulation - In treatment you allow permissive hypertension (preventing hypoperfusion) - But you must keep BP from going too high to avoid reperfusion haemorrhage (ESPECIALLY after tPA is given) Haemorrhagic stroke -Anticoagulants and antithrombolytics are contraindicated as this is a bleed! -SAH Medical: nimodipin (a CCB) to prevent vasospasm in blood vessels damaged by the haemorrhage Surgical: treatment is surgical. You clip or block off the blood vessel. Craniotomy to relieve pressure BP: To keep BP sufficiently low (no higher than 140, see below), you give the beta blocker labetalol or the CCB nicardipine. Raised ICP: Head of bed elevation to 30° Mannitol Brief hyperventilation (causes cerebral vasoconstriction) NPO (no food or drink until formal swallow evaluation!)

Answer 133

Complication of ischaemic stroke treatment: Giving tPA can potentially cause serious bleeding, so giving it to someone with an ischaemic stroke when the blood vessels are damaged can lead to haemorrhagic stroke!

Answer 134

Oxygen Subcutaneous sumatriptan Prophylactic: verapamil

Answer 135

``` INR >1.7 PTT >15s BP>185/110 Platelet <100,000 Heparin in last 48hrs Surgery past 14 days GI haemorrhage last 21 dats Previous ischaemic stroke Head trauma ``` SHOULD ONLY GIVE ASPIRIN 24HRS AFTERWARDS TO AVOID RISK OF BLEEDING BP should be below 185/110, and should be kept below 180/105 for at least 24hr. ---------------------------------- If no tPA is given or if the patient has cardiac disease, BP kept below 220/110. ------------------------------------- In haemorrhagic stroke keep the BP high enough to perfuse brain but systolic pressure must be kept below 140 to avoid another bleed

Answer 136

A transient ischaemic attack (TIA) is a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction. The majority of TIAs resolve within the first hour, and diagnostic imaging allows recognition that some events with rapid clinical resolution are associated with permanent cerebral infarction. NOT LEFT WITH ANY NEUROLOGICAL DEFICIT OR SYMPTOMS

Answer 137

Rapid access TIA (in 24hrs) clinic: CT/MRI and carotid USS and or MRA/CTA FBC, electrolytes, glucose, lipids, clotting ECG, echo (to look for atrial and ventricular clots) and send home with holter (ecg over 24hrs) Angiography and carotid ultrasound. NO VISIBLE INFARCTS SHOULD BE PRESENT ON CT/MRI (but you might be able to see little ischaemic areas with TIA) MRI is gold standard

Answer 138

Work out ABCD2 score, figures out the risk of having a subsequent stroke following a TIA ``` Age Blood pressure Clinical features Duration of TIA Diabetes II ``` Score 1-3 no hospitlisation unless in AF Moderate score (4-5) or high score (6-7) should be hospitalised immediately and monitored for a day. No immediate treatment required

Answer 139

Future stroke clearly highly likely

Answer 140

Headache, vomiting, papilloedema Cushing's triad (HTN, bradycardia and irregular respirations)

Answer 141

Stroke could've emerged from heart, so do an ECG + ambulatory cardiac monitoring. If there is evidence of AF then assume there is a blood clot from here, give anticoagulation therapy (warfarin AND rivoroxaban) + Long term antithrombotics (daily aspirin) (these should also be given to people with valvular disease, endocarditis or MI) Those with severe intracranial stenosis (based on MRI/CT angiography) should have clopi for 90 days. Furhter investigations; - Echocardiography to locate source for embolic stroke. - Carotid artery stenosis - Hypercoagulable studies (protein C/S, plasminogen, antithrombin III, antiphospholipid antibodies. All associated with thrombosis)

Answer 142

40-69% stenosis= lifestyle changes 70%+= stent or carotid endarectomy

Answer 143

MRI or CT 4-8wks after the stroke as the blood will be mostly reabsorbed and you might be able to see an underlying vascular malformation/brain tumour Control HTN, diabetes Quit smoking Eating well, exercise regularly

Answer 144

Gradual onset over five years No other associated symptoms Around 50% with essential tremor Symmetrical Worse when lifting a cup

Answer 145

The actual tremor: - Pill rolling character - Low frequency - Asymmetrical -------------- Gradual onset over five years Resting (won't be worse with lifting a cup for example) Usually not hereditary. But

Answer 146

Bradykinesia Tremor Rigidity Postural instability

Answer 147

- Onset at any age - Family history - Worse with movement (it actually gets better with alcohol weirdly)

Answer 148

Pyramidal tract (UMN). More tone in the upper part of the movement. "clasp nice" Extra-pyramidal lesion. Lead pipe rigidity. And cog wheel because you get tremor on top.

Answer 149

Watchful waiting Propanalol Reduce caffeine Primidone

Answer 150

Bilateral Pressing/tightening in character Pericranial tenderness

Answer 151

Simple analgesia Do NOT offer opioids Identify co-morbidities (stress, sleep issues) If chronic: amitriptyline and acupuncture!

Answer 152

One-sided headache in ophthalmic nerve distribution region with autonomic symptomatology

Answer 153

Unknown Types: 1) Episodic: Daily episodes over 6–12 weeks; “clusters” followed by remission period up to 12 months 2) Chronic: Episodes without substantial remission period Risk factors: - Male - Stressful periods, allergic rhinits, sexual intercourse, tobacco, excessive alcohol

Answer 154

Headache that is one-sided, sharp, stabbing and orbital/supraorbital, temporal head pain Autonomic symptoms: -Ipsilateral conjunctival hyperemia with lacrimation, nasal discharge, mioisis, oedema and drooping eyelid 1-8 episodes per day lasting 5 mins to 3hrs Restlessness, agitation, suicidal ideation

Answer 155

CT/MRI --> exclude possible cranial lesions. Diagnosis requires each of the following: - Five unilateral/orbital/supraorbital/temporal attacks; 1–8 episodes daily, ≤ three hours - Agitation/restlessness - ≥ one autonomic symptom on same side as headache

Answer 156

The Tensilon test involves administering a very short-acting acetylcholinesterase inhibitor to diagnose myasthenia gravis by demonstrating by a rapid improvement in muscle weakness.

Answer 157

Subclavian steal syndrome is a phenomenon in which stenosis of the subclavian artery proximal to the origin of the vertebral artery results in blood being ‘stolen’ from the brain by retrograde blood flow down the vertebral artery and into the arm. Leads to blackout Occurs when increased demand for blood in the arm

Answer 158

Cervical rib, atherosclerosis, takayasu's arteritis

Answer 159

Hemisection of the cord is also known as Brown–Séquard syndome. This results in ipsilateral paralysis and loss of light touch and vibration sensation and contralateral loss in pain and temperature below the point of the lesion. The spinothalamic tracts cross at the level of the cord, so sensation to pain and temperature is lost in the contralateral limbs

Answer 160

Low pressure CSF headache. If the patient had an epidural during c section, then the catheter may have passed through the dura, creating a hole, and causing a leakage of CSF and a low pressure headache. It is worse on standing and better on lying down. Radiating down into the neck. Terrible pain. Photophobia and neck stiffness

Answer 161

Multiple slcerosis

Answer 162

-Broca's area. Broca’s area, located in the frontal lobe of the dominant hemisphere, is responsible for speech production. -Wernicke's area. Damage to Wernicke’s area results in the inability to understand language, however, patients will be able to produce fluent, but nonsensical, speech -The arcuate fasciculus connects Wernicke’s and Broca’s areas. Lesions of the arcuate fasciculus results in intact language comprehension and fluent speech production;

Answer 163

They should be given 300mg aspirin immediately, and assessed urgently within 24hrs. Patients with confirmed TIAs should then continue aspirin (or clopi) and be given secondary prevention meds (antihypertensives and statins)

Answer 164

Viral meningitis- enteroviruses e.g. poliovirus, cocksackie A) and herpes viruses (HSV, VZV, EBV) Viral encephalitis- HSV

Answer 165

symptoms are often less severe and do | not progress as quickly in viral meningitis

Answer 166

Diagnosed on basis of CSF analysis via an LP. Therefore, a CT scan is the first most appropriate investigation

Answer 167

Bacterial- cloudy/turbin Viral- usually clear TB-fibrinous

Answer 168

Bacterial- neutrophil Viral- lymphocyte TB- lymphocyte

Answer 169

High in all

Answer 170

Bacterial- low Viral- normal TB- low

Answer 171

Wet, wacky and wobbly Urinary incontienence, Confusion/dementia Gait disturbance

Answer 172

Obstructive hydrocephalus can also cause confusion, however, it usually presents with a rapid drop in consciousness (if acute) and signs of raised ICP (e.g. Cushing’s triad, headache that worsens when lying down),

Answer 173

An autoimmune condition associated with antibodies forming against nicotinic acetylcholine receptors at the NMJ, resulting in weakness

Answer 174

Impairment of neuromuscular junction transmission, due to auto-antibodies against the nicotinic acetylcholine receptor (nAChR). A paraneoplastic subtype (Lambert–Eaton myasthenic syndrome) is caused by auto-antibodies against pre-synaptic calcium ion channels impairing acetylcholine release. Associated with other autoimmune conditions e.g. pernicious anaemia and thymoma development. (75% have thymoma, so breakdown of immune tolerance is thought to arise in thymus)

Answer 175

In younger ages, more common in females Equal gender distribution at middle age

Answer 176

MG: Muscle weakness that worsens WITH REPETITIVE use or towards end of day Lambert eaton: muscle weakness IMPROVES with repeated use. Ocular: droopign eyelids, diplopa Bulbar symtpoms: facial weakness (myasthenic snarl), disturbed hypernasal speech, difficulty smiling, chewing or swallowing (nasal regurgitation of liquids)

Answer 177

May be generalised, bular, or ocular. EYES: Bilateral ptosis. Complex opthalmoplegia. Test for ocular fatigue by asking them to sustain upward gaze for 1 minute and watch for progressive ptosis. Ice test (ptosis improves >2mm from baseline when ice packs placed) Bulbar: reading aloud may provoke dysarthria or nasal speech after 3 mins Limbs: test power of muscle before and after repeated use (20 repetitions)

Answer 178

1st investigations: - Serum acetylcholine receptor antibody analysis - MuSK antibodies - Pulmonary function tests (respiratory involvement) Blood: - Serum acetylcholine receptor antibody (present in 80%) - TFT (may be ass hyperthyroidism) - Atypical features may warrant testing of anti-MUSK (uncommon variant) and anti-VGCC Ab (for Lambert eaton) Tensilon test: Short acting anti-cholinesterase increases ACh causeing rapid and transient imporvement in clinical deatures. Avoided due to risk of bradycardia. Nerve conduction study: May show decrement of muscle action potential. May differentiate between MG and LE. EMG: single fibre EMG may demonstrate "jitter" (variability in latency from stimulus to muscle potential) indicating fluctuation at NM junction CT thorax/CXR to visualise thymoma in mediastinum or malignancy in the lung (LE)

Answer 179

Like a X-ray of the skull from a supero-posterior perspective. Shows occipital bone fractures well

Answer 180

In particular the presence of a fixed dilated pupil is highly suggestive of significant raised intracranial pressure requiring urgent neurosurgical intervention It suggests transtentorial herniation (coning)

Answer 181

F IV contrast is not indicated in the head injury setting.

Answer 182

indicating there must be a skull fracture

Answer 183

Subdural haematomas are much more common than extradural haematomas, and they are usually due to tearing of a bridging vein from the cerebral cortex and a draining venous sinus. Extradural haematomas (EDH) are located outside the dura and are most commonly due to tearing of the middle meningeal artery due to a fracture

Answer 184

It can be acute, chronic or acute on chronic.

Answer 185

Chronic SDH will often present with a vague history with symptoms such as fluctuating conciousness, headache, personality change, confusion. The initial traumatic event may not be remembered or will have been trivial. MUCH MORE COMMON IN: 1) ELDERLY 2) THOSE SUSCEPTIBLE TO MULTIPLE FALLS e.g. alcohol dependent people, people with epilepsy AND 3) THOSE ON ANTICOAGULATION) A CT scan will show a crescent-shaped haematoma over one hemisphere and blood will tend to extend along he falciform ligament and over the tentorium cerebelli.

Answer 186

A biconvex shape is seen with an EDH where the blood is limited by the dural attachments.

Answer 187

So you can get isolated ocular MG

Answer 188

Tests for AchR antibodies are present in 95% of patients with generalised MG, but only in approximately 50% of patients with ocular MG (in which only the eyelids and extraocular muscles are affected)

Answer 189

These are when, for example you hit the back of your head, but the brain hits the front of the skull, resulting in bruises there

Answer 190

White spots in the brain, which should usually be grey

Answer 191

NSAIDs and paracetemol Prochlorperazine Opioid is a bad choice (causes headaches and nausea)

Answer 192

Epilepsy So you need to do seizure prophylaxis

Answer 193

F.... the group does worse with more infection Tranexamic acid should be given in moderate bleeds

Answer 194

Occipiptal lobe fracture can cause occlusive thrombus in a venous sinus, which reduces venous return from the brain. You do a CTV to look for thrombosis

Answer 195

1. Reduce CSF in the head (can put in a drain) 2. Reduce blood (sit up, remove collars (and NM block), make sure not constipated, mannitol (or hypertonic saline is better as mannitol causes diuresis) 3. Reduce brain volume (by reducing brain activity, NM blocker, anti-seizure)

Answer 196

The skull fracture down the midline can cause superior saggital sinus tear

Answer 197

Cold, metabolic acidosis, coagulopathy

Answer 198

Cauda equina syndrome is a severe form of lumbar spinal stenosis caused by sudden compression of the nerves of the cauda equina. Spinal cord stenosis is a narrowing of the spinal canal, most commonly occurring in the lumbar spine. An important distinction to take note of is that acute cord compression (such as cauda equina syndrome) causes lower motor neuron signs, whereas gradual cord compression (as in this patient) causes upper motor neuron signs.

Answer 199

equina. It presents acutely with urinary retention and lower back pain. Examination findings include lower motor neuron signs, perianal numbness and lax anal tone.

Answer 200

This includes osteophytes (osteoarthritis/paget's), disk herniation, tumours, ligamentum flavum hypertrophy

Answer 201

Myotonic seizures

Answer 202

Upper motor neuron (UMN) lesions (e.g. a stroke) will have an acute phase during which you get ‘loss of function’ signs (e.g. flaccid paralysis). Then, there will be an increase in abnormal motor function caused by the loss of descending inhibitory inputs from the central nervous system. This results in increased muscle tone (spasticity)

Answer 203

Fasciculations are visible twitches in the muscle, caused by damaged motor units firing spontaneous, uncoordinated action potentials. Fibrillations are twitches of individual muscle fibres that can be observed using electromyography but are not visible to the naked eye.

Answer 204

Lumbar spinal stenosis

Answer 205

Type 1 mainly causes peripheral manifestations such as café-au-lait macules (‘coffee-cloured, flat skin lesions’), axillary freckling, neurocutaneous fibromas, phaeochromocytomas and renal artery stenosis.

Answer 206

Type 2 has mainly central features, such as bilateral vestibular schwannomas, meningiomas and gliomas.

Answer 207

Hypotension and arrhythmia

Answer 208

``` Bony metastasis Myeloma Epidural abscess Disc prolapse Epidural haematoma Primary sacral tumour e.g. chordoma ```

Answer 209

This patient needs urgent same day assessment by spinal surgeon, imaging and then surgical decompression as appropriate – this must be done within hours and even waiting until the next day may allow irreversible damage and paralysis to occur.

Answer 210

Cauda equina compression causes flaccid paralysis with loss of reflexes. Cord compression usually causes spastic paralysis with brisk reflexes. Both cause sensory and power loss.

Answer 211

The diagnosis of MS is heavily based on the clinical history and there is no straight-forward diagnostic test. However, CSF electrophoresis may show oligoclonal bands and an MRI scan may show sclerotic plaques that may or may not correspond with the neurological symptoms experienced by the patient. Bence-Jones proteins are immunoglobulin light chains which are found in the urine of patients with multiple myeloma. High CSF protein is a feature of Guillain-Barré syndrome. Xanthochromia is a ‘straw-coloured’ discoloration of the CSF seen when performing a lumbar puncture.

Answer 212

Xanthochromia will be present from 12 hours to 12 days after onset of a subarachnoid haemorrhage.

Answer 213

Autosomal dominant condition, mutation in tumour suppressor gene. Tumours commonly include haemangioblastomas occuring in cerebellum and retina, clear cell renal carcinoma, phaeo, pancreatic islet and endolympohatic sac tumours

Answer 214

Wilson's disease is an autosomal recessive ``` genetic disorder in which copper accumulates in tissues; this manifests as neurological or psychiatric symptoms and liver disease. If there are neurological symptoms , MRI of the brain is usually performed; this shows hyperintensities in the basal ganglia . ```

Answer 215

Apraxia is a disorder of higher-order motor control leading to difficulty performing skilled movements. It is not due to a problem with the primary motor systems or due to a lack of understanding. Issues with planning and initiation

Answer 216

F extra-ocular movement and visual perimetry testing reveal abnormalities, but visual acuity testing does not Frequent accompanying symptoms of pseudotumor cerebri include: Visual field loss - manifesting as enlargement of the blind spot Extraocular movement disturbances most frequently due to abducens palsy in 1/3 of patients Pulsatile tinnitus .

Answer 217

Conus medullaris

Answer 218

- Genitals - Internal and external anal sphincter - Detrusor vesicae - Leg muscles

Answer 219

Knee and ankle reflexes, skin sensation for legs and pelvis

Answer 220

Compression, trauma or damage to multiple nerves of the cauda equina. Lumbar disc herniation is most common Spinal stenosis (narrowing of the vertebral foramen)- ank spond, sponylolisthesis Trauma to spine (can directly damage nerves, or cause compression due to haematomas) Growth in spinal cord (abscess, cyst, tumour)

Answer 221

It's essentially a similar process, but the herniation is usually larger with cauda equina, and affectes the nerves going to the muscles controlling bladder and sphincter

Answer 222

Can be congenital, or acquired. Acquired cause is ankylosing spondylitis where bones remodel causing intervertebral disc ossification and thus narrowing of spinal canal Another cause of spinal stenosis (and thus cauda equina) is spondylolithesis

Answer 223

When a vertebra is displaced by tauma, surgery of degenerative disc spinal disease Most common: anterolisthesis

Answer 224

Reduced bowel or bladder control Reduced tone of anal sphincter/muscle wall of bladder Reduced sexual function Saddle anaesthesia 1 or both legs can have muscle weakness, loss of knee and ankle reflexes and paraplegia Sciatic PAIN

Answer 225

Usualyl based on pattern of sensory and mot`or nerve findings CONFIRMED BY MRI/CT SCAN

Answer 226

Genetic condition- AUTOSOMAL DOMINANT. Affect cells of neural crest origin, resulting in development of multiple neurocutaneous tumours

Answer 227

``` Cafe au lait spots Axillary/inguinal freckling Fibromas Eye hamartomas (Lisch nodules) Skeletal abnormalities (sphenoid wing dysplasia) Phaeochromocytoma/+ve family history OT: optic tumour (optic nerve glioma) ```

Answer 228

Characterized by schwannomas, e.g. bilateral vestibular schwannomas (acoustic neuromas), peripheral/spinal schwannomas, meningiomas, gliomas, cataracts

Answer 229

Tumour suppressor genes

Answer 230

Mutations in NF1 gene (chromosome 17) which encodes neuroﬁbromin (a GTPase activating protein). Mutations in neuroﬁbromin result in excessive activity of the protooncogene p21-ras.

Answer 231

Type 2 NF: Mutations in NF2 (chromosome 22) which encodes merlin (or schwannomin).

Answer 232

Type 1 NF: Skin lesions, learning difﬁculties (in 40%), headaches, disturbed vision (optic gliomas, in 15%), precocious puberty (may indicate lesions of the pituitary from optic glioma involving the chiasm).

Answer 233

Type 2 NF: Hearing loss, tinnitus, balance problems, headache, facial pain or numbness.

Answer 234

Type 1 NF: >5 cafe au lait macules of >5mm (pre-pubertal individuals) or >15mm (post-pubertal individuals), neuroﬁbromas (appear as cutaneous nodules or complex plexiform neuromas), freckling in armpit or groin, Lisch nodules (hamartomasoniris), spinal scoliosis.

Answer 235

Type2: NF: Few or no skin lesions, sensorineural deafness with facial nerve palsy or cerebellar signs if schwannoma large (see Acoustic neuroma).

Answer 236

MRI/CT brain to look for optic gliomas (type 1) or to exclude other masses Biopsy Genetic testing (confirms the diagnosis)

Answer 237

Alpha-synuclein

Answer 238

Posttraumatic ``` hydrocephalus is a frequent and serious complication that follows a traumatic brain injury . It may present as normal pressure hydrocephalus or as increased intracranial pressure . The onset of acute posttraumatic ``` hydrocephalus is at least 2 weeks after the head trauma has occurred

Answer 239

Degeneration of the dorsal and lateral columns. Vibration and touch are diminished with paresthesia, gait ataxia, and weakness.

Answer 240

B12 deficiency (coeliac is RF)--> subacute combined degeneration In SCD, the extremeties are affected symmetrically usually beginning with the lower limbs. eakness, clonus, and cerebellar ataxia can also occur.

Answer 241

Abortive: - Limit stimuli and activity - MILD TO MODERATE: NSAIDs - SEVERE: triptains or ergotamine (don't combine). Can combine with NSAIDs. Avoid opioids - Add anti-emetic (IV or IM) if N&V present Prophylaxis: - Avoid triggers, acupuncture - Pharm: b blocker, tricyclic antidepressants, anticonvulsants, CCBs

Answer 242

Coronary artery disease Peripheral artery disease Hypertension Pregnancy and breastfeeding

Answer 243

5-HT1 receptor agonist → vasoconstriction of (dilated) cranial and basilar arteries

Answer 244

Frequent attacks (e.g., ≥ 3 attacks/month) Long-lasting attacks (e.g., > 12–24 hours) or aura Abortive therapy fails or is contraindicated

Answer 245

Temporary blood pressure increase (very common) Paresthesia and sensation of cold in the extremities Dizziness, malaise, flashes Frequent intake (≥ 10x/month) can lead to headaches Coronary ischemia (rare)

Answer 246

HLA-DR2 genotype | .

Answer 247

aniscoria is indicative of an | uncal herniation

Answer 248

a subarachnoid hemorrhage leading to increased intracranial pressure

Answer 249

f. Herniation can also occur in the absence of high ICP when mass lesions such as hematomas occur at the borders of brain compartments. In such cases, local pressure is increased at the place where the herniation occurs, but this pressure is not transmitted to the rest of the brain, and therefore does not register as an increase in ICP.

Answer 250

Cingulate herniation occurs when the cingulate gyrus ``` herniates beneath the falx cerebri . This can lead to compression of the anterior cerebral artery . ```

Answer 251

``` Cerebellar tonsillar herniation occurs when the cerebellar tonsils herniate down through the foramen magnum . This can lead to compression of the medulla and lead to dysfunction of the respiratory centers. ```

Answer 252

Pilocarmine, a muscarinic agonist

Answer 253

``` Tabes dorsalis is the loss of coordination of movement due to demyelination of nerves in the dorsal column , and is typically a complication of neurosyphilis . ```

Answer 254

``` Risk factors include brain atrophy, as can be seen in elderly patients or those with chronic alcohol abuse , as well as low- coagulation states. ```

Answer 255

Acute (1-3d, hyperdense on CT) Subacute (4d-2wks, isodense on CT) Chronic (>2wks, hypodense on CT).

Answer 256

``` Bacterial meningitis caused by Neisseria meningitidis is best treated by a 3rd generation cephalosporin such as ceftriaxone .Empirical therapy of community-acquired suspected bacterial meningitis in children and adults should include a combination of dexamethasone , a third- or fourth-generation cephalosporin , and vancomycin . ``` ``` Gram +ve: Vancomycin is used to treat meningitis caused by gram-positive organisms such as Streptococcus pneumoniae , except for ``` Listeria monocytogenes which is treated with ampicillin .

Answer 257

``` Hemispatial neglect is a syndrome that occurs after an individual sustains a brain lesion , and is characterized by agnosia of the contralateral half of the world. It is most often a result of damage sustained to the nondominant parietal cortex through a traumatic brain injury , neoplasm, aneurysm , or stroke . ```

Answer 258

Damage to the dominant parietal cortex results in neurological ``` deficits such as acalculia , agraphia , finger agnosia , and left-right disorientation. ``` ``` With non-dominant, outside of their hemispatial neglect , the patient is neurologically intact. ```

Answer 259

``` Bilateral amygdala damage leads to Kluver-Bucy syndrome , characterized by disinhibited behavior such as hypersexuality , hyperorality, and hyperphagia . It is associated with herpes simplex virus -1 encephalitis . ```

Answer 260

Primary tumours arising from any of the brain tissue types.

Answer 261

Headache or vomiting (raised intracranial pressure), epilepsy (focal or generalized), focal neurological deﬁcits (dysphagia, hemiparesis, ataxia, visual ﬁeld defects, cognitive impairment), personality change.

Answer 262

Para sagittal region

Answer 263

Cerebellopontine angle

Answer 264

Olfactory groove

Answer 265

Cavernous sinus

Answer 266

Foster Kennedy syndrome

Answer 267

Pituitary fossa

Answer 268

Parinaud's syndrome (pineal region)

Answer 269

Meningioma (benign)

Answer 270

Medulloblastoma: Invasive midline cerebellar tumour in children.

Answer 271

Vascular tumours, often in the cerebellum.

Answer 272

CT head But MRI is the better imaging

Answer 273

: Higher sensitivity. Diffusion-weighted-imaging and MR spectroscopy can be helpful in characterizing lesion without biopsy. Functional MRI may be necessary if the lesion is located in dominant hemisphere for surgical planning --------------------- A definitve diagnosis is based on histologic and molecular characteristics

Answer 274

Most common type of benign pediatric primary brain tumor: pilocytic astrocytoma Most common malignant pediatric primary brain tumor: medulloblastoma

Answer 275

Most common benign primary brain tumor in adults: meningioma | Most common malignant primary brain tumor in adults: glioblastoma multiforme

Answer 276

Primary CNS tumors do not metastasize to organs outside the CNS. They spread within the CNS: -Leptomeningeal metasteses (spread to meninges) -Drop metastases (intradural extramedullary spinal metastases that are typically found in the lower thoracic and lumbar regions)

Answer 277

Majority are supratentorial (opposite to kids)

Answer 278

T. Glioblastoma is a type of astrocytoma. But it's highly malignant so it's by default a grade IV tumour

Answer 279

This is the glioblastoma (a highly malignant astrocytoma) It's got this pattern because it's so fast growing, that `what you get is a central area of necrosis (because it grows faster than angiogenesis can keep up with), but a peripheral area of viable cells.

Answer 280

Meningioma Psammoma bodies (calcifications) may also be present

Answer 281

Cells in the arachnoid mater, called the arachnoid cap cells Meningiomas form in the parasagittal regions and on the surface of the brain UNDER the dura mater.

Answer 282

Graded I-III. Slow growing.

Answer 283

Can occur in the brain or spinal cord. In adults typically occur in frontal lobes as these neurons are the most heavily myelinated

Answer 284

Classifed grade II-III. Relatively slow growing but can become malignant

Answer 285

Grade III oligodendroglioma

Answer 286

Grade II oligodendroglioma

Answer 287

This is likely to be a haemangioblastoma.

Answer 288

They are grade 1 (slow growing tumours) Rare in adults (it's an infratentorial tumour, whereas most adult tumours are supratentorial)

Answer 289

Pineallomas, ependymomas, medulloblastomas

Answer 290

MENINGIOMA: Spindle cells in whorls with psamomma bodies SCHWANNOMA: Spindle cells in palisades Antoni A tissue) alternating with myxoid areas (Antoni B tissue) S-100 positive

Answer 291

Pituitary adenoma

Answer 292

Cerebellopontine angle (infratentorial) | Unilateral deafness, facial weakness, then unilateral ataxia and hemifacial sensory impairment

Answer 293

``` Lung cancer (most common) Breast cancer Malignant melanoma Renal cell carcinoma Colorectal carcinoma ```

Answer 294

NON-CONTRAST CT head

Answer 295

``` Anton syndrome, which is defined as cortical blindness due to bilateral occipital lobes damage that can occur in instances of stroke or trauma. Pupillary reactions are normal, and bilateral macular sparing may preserve central (tunnel) vision. With more extensive lesions, denial of blindness may occur. ``` They insist they can see

Answer 296

``` In adults, acute or chronic infections of the sinuses can spread into the orbit causing orbital cellulitis . ```

Answer 297

``` Valproic acid is an anti-epileptic drug that is contraindicated in pregnancy due to teratogenic effects causing neural tube defects , and tends to cause polycystic ovarian syndrome in women with seizures . ```

Answer 298

``` Adverse effects of levetiracetam include drowsiness , mild psychiatric disturbances, and rarely Stevens-Johnson syndrome and toxic-epidermal necrolysis ```

Answer 299

``` Adverse effects of this medication include drowsiness , nausea , headache , and more seriously, agranulocytosis ```

Answer 300

Intention tremors occur at the end of guided, intentful movements. They are often caused by a lesion to the cerebellar hemisphere , ipsilateral to the affected extremity

Answer 301

``` Locked-in syndrome is a condition caused by a stroke involving the basilar artery ``` ``` Basilar artery supplies the pons , lower midbrain , and medulla, and thus its infarction affects the corticospinal and corticobulbar tracts while sparing the oculomotor nerves. ``` So there is quadraplegia and loss of voluntary mouth, tongue and facial movements, with preserved consciousness and vertical eye movement.

Answer 302

``` Infarction of the anterior spinal artery results in medial medullary syndrome , characterized most notably by its effects on the lateral corticospinal tract ( contralateral ``` ``` paralysis of upper and lower extremities), medial lemniscus (decreased contralateral ``` ``` proprioception ), and hypoglossal nerve in the caudal medulla ( ipsilateral tongue motor dysfunction ). ```

Answer 303

``` Infarction of the posterior cerebral artery results in deficits to the occipital and visual cortices , and thus patients present with contralateral ``` ``` hemianopia with macular sparing (as the portion of the visual cortex responsible for macular, or central, vision is also supplied by the middle cerebral artery ) ```

Answer 304

``` Infarction of the posterior inferior cerebellar artery results in lateral medullary syndrome , also called Wallenberg syndrome , characterized most notably by its effects on the nucleus ambiguus (controls the soft palate , larynx , and pharynx ). Patients are unable to swallow ( dysphagia ) and have a hoarse voice. Ipsilateral ``` Horner syndrome is also common.

Answer 305

Bilateral facial nerve palsy is often associated with untreated Lyme disease and GBS

Answer 306

This occurs when there is inflammation and fibrosis of the arachnoid granulations impairing resorption of CSF This is most often seen following subarachnoid or interventricular hemorrhage or meningitis . It can however occur in the absence of an underlying observable cause, named idiopathic normal pressure hydrocephalus .

Answer 307

A subdural haemorrhage (SDH) is a collection of blood that develops between the surface of the brain and the dura mater. Acute- within 72hrs Subacute- 3 to 30 days Chronic- after 3 weeks

Answer 308

Trauma causing rapid acceleration and deceleration of the brain results in shearing forces which tear veins ("bridging veins") that travel from the dura to the cortex. Bleeding occurs between the dura and arachnoid membranes.

Answer 309

Acute: Tend to occur in younger patients/associated with major trauma (5–25% of cases of severe head injury). More common than extradural haemorrhage. Chronic: More common in elderly, studies report incidence of 1–5 per 100000.

Answer 310

Acute: History of trauma with head injury, patient has reduced conscious level Subacute: Worsening headaches 7–14 days after injury, altered mental status Chronic: Can present with headache, confusion, cognitive impairment, psychiatric symptoms, gait deterioration, focal weakness, seizures. May not be a Hx of fall or trauma (have low index of suspicion in elderly and alcoholics)

Answer 311

Acute: reduced GCS. Ipsilateral fixed dilated pupil (compression of the ipsilateral 3rd nerve parasympathetic fibres), pressure on brainstem: reduced consciousness, bradycardia. Chronic: neuro exam may be normal. Or focal neuro signs (III or VI nerve dysfunction, papilloedema, hemiparesis or reflex asymmetry)

Answer 312

CT non-contrast: Crescent or sickle shaped mass, concave over brain surface (compared to extradural which is lentiform). CT appearance changes with time. Acute subdurals are hyperdense, becoming isodense over 1–3weeks (such that presence maybe inferred from signs such as effacement of sulci, midline shift, ventricular compression and obliteration of basal cisterns); and chronic subdurals are hypodense (approaching that of CSF). MRI-brain: Has higher sensitivity especially for isodense or small SDHs.

Answer 313

Acute: ALS protocol. f signs of raised ICP, head elevation and consider osmotic diuresis with mannitol and/or hyperventilation. Once stabilised, obtain CT-head. Conservative: esp woth small/minimal midline shoft (SDH<10mm thickness, and midline shift <5mm) Surgical: Prompt Burr hole or craniotomy and evacuations for symptomatic subdurals >10mm with >5mm midline shift (better outcome if within 4h). ICP monitoring device

Answer 314

If symptomatic or there is mass effect on imaging, surgical treatment with Burrhole or craniotomy and drainage (a drain may be left in for 24–72h). Asymptomatic SDH without signiﬁcant mass effect is best managed conservatively with serial imaging to monitor for spontaneous resorption. Haematomas that have not fully liqueﬁed may require craniotomy with membranectomy.

Answer 315

Raised ICP, cerebral oedema pre-disposing to secondary ischaemic brain damage, mass effect (transtentorial or uncal herniation).

Answer 316

T Chronic have better outcome, reﬂecting lower incidence of underlying brain injury, with good outcomes in 3/4 of those treated by surgery.

Answer 317

Characterised by reduced sympathetic innervation to the head Leads to miosis, anhidrosis and partial ptosis

Answer 318

Most cases of HS are idiopathic, but conditions such as brainstem stroke, carotid dissection, and neoplasm are occasionally identified as the cause of HS. CENTRAL: Brainstem stroke (Wallenberg), cervical spine injury (Brown Sequard syndrome), brain tumorurs, MS, lateral medullary syndrome etc. PRE-GANGLIONIC: breast/lung cancer (pancoast tumour), iatrogenic, lymphadeniopathy, cervical rib POST GANGLIONIC: Dissection of the internal carotid artery, cluster headache, tumor, HZV

Answer 319

Appropriate imaging modalities should be obtained emergently and may include MRI and MR angiography or CT angiography of the neck. Conventional angiogram remains the gold standard. Patients should be treated promptly by anticoagulation under the supervision of a neurologist.

Answer 320

Chest xray and then contrast CT/MR scan

Answer 321

``` Trigeminal neuralgia can be caused by compression from an anatomical variation of the superior cerebellar artery . ` Trigeminal neuralgia can result from a redundant loop of the superior cerebellar artery that impinges on the trigeminal root. ```

Answer 322

``` First-line treatments for an acute attack include oxygen and triptans . Verapamil 's mechanism of action in the primary prevention of cluster headaches is still unclear, though one leading theory suggests that this medication may affect central neuronal pathways, particularly those in the hypothalamus . ```

Answer 323

It starts hyperdense. As the haematoma ages, it becomes isodense and then in a few weeks hypodense (similar to CSF).

Answer 324

Rebleeding into the haematoma is common and density can appear mixed

Answer 325

The dilated ventricles fits with hydrocephalus But hydrocephalus does not involve expansion of the subarachnoid space Therefore something else is going on to make the subarachnoid space expand, and that's cerebral atrophy Hydrocephalus ex vacuo, also known as compensatory enlargement of the CSF spaces, is a term used to describe the increase in the volume of CSF, characterised on images as an enlargement of cerebral ventricles and subarachnoid spaces, caused by encephalic volume loss.

Answer 326

Acute drop in conscious level. Diplopia. Impaired GCS, papilloedema, VI nerve palsy (false localizing sign of increased ICP). In neonates, the head circumference may enlarge, and "sunset sign" (downward conjugate deviation of eyes).

Answer 327

``` hyperintensity in the right temporal lobe which is specific to herpes simplex encephalitis . ```

Answer 328

Bleeding and accumulation of blood into the extradural space

Answer 329

Head trauma causes fracture (most commonly squamous temporal bone as this is the thinnest part of cranial vault) Ruptures middle meningeal artery Arterial bleeding causes rapid accumulation of blood and strips the dura from the inner table of the skull. Increased ICP and compression of underlying brain parenchyma

Answer 330

Head injury with temporary loss of conscioussness, followed by lucid interval and then development of progressive deterioration on consicousness level

Answer 331

Signs of scalp trauma or fracture Headache Reducing GCS Signs of raised ICP (dilated unresponsive pupil on the side of the injury) Abnormal posturing (decortical and decerebrate) and cushing's sign (rising BP and bradvardia) are late signs

Answer 332

Urgent CT scan: Diagnostic and identifies location of haematoma Arterial bleed produces convex/lens-shaped haematoma. Signs of raised ICP incllude midline shift, compression of ventricles, obliteration of basal cisterns and culcal effacement

Answer 333

children who have seizures are more likely to be infected by Streptococcus pneumoniae and Haemophilus influenza than meningococcus

Answer 334

First line treatment is with ethosuximide, valproate or lamotrigine.

Answer 335

. The MMSE is the most widely used screening test for cognitive function and a score <24 is widely accepted as abnormal.

Neurology Flashcards

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