Week 12 Neuro Flashcards

Question

Peripheral neuropathy

Answer 1

Damage to peripheral nerves Presntation depends on which fibres affected: Motor fibres - weakness Large fibres - sensory ataxia (due to loss of proprioception), numbness/tingling (loss of light touch), vibration sense, Small (myelinated/unmyelinated) sensory fibres) - impaired pin prick sensation, temp sensation Autonomic: postural hypotension, abnormal sweating Causes: diabetes, hypothyroidism, B12 deficiency

Answer 2

Diffuse involvment of peripheral nerves \>50 yrs Symmetrical Starts in toes/feet and moves proximally No significant sensory ataxia Weakness is distal and mild Causes: Diabetes, Alcohol, Nutritional (B12 deficiency), Drugs e.g. Isoniazid, Immune mediated e.g. RA, lupus

Answer 3

Post-infectious autoimmune neuropathy Targets myelin sheath Gradual onset Medical Emergency Causes: campylobacter, EBV - Flaccid, quadraparesis (weakness of all 4 limbs), areflexia (absent reflexes) +/- Respiratory (e.g. SOB) bulbar duysfunction (e.g. dysphagia), autonomic involvement (tacycardia, HTN) Treated with IV IG or aphresis

Answer 4

Clinical features of muscle disorders: Proximal limb weakness (difficult rasining arms above head, lifting up from seat) Facial weakness Eyes: ptosis Bulbar: dysarthria (difficulty speaking), dysphagia (difficulty swallowing) Respiratory - breathless esp. when lying flat (as nerves innervating diaphragm isn't working properly) Causes of muscle disease: DMD/BMD Inflammatory muscle disoders: Polymyositis NMJ disorders: Myasthenia gravis, Lambert Eaton syndrome

Answer 5

Autoimmune disoder where autoantibodies agianst AchR at post-synaptic NMJ. Decreased generation of muscle APs causing skeletal muscle weakness Assoc with other autoimmune disorders, and thyoma Young women, old men **Symptoms:** **Fatiguable weakness** of ocular, bulbar, respiratory and/or limb muscles Ptosis, diploplia, dysphagia, dysarthria, proximal muscle weakness No sensory loss **Investigations:** serum anti-achetylcholine receptor antibodies (AchR) (85% present) Abnormal single fibre EMG, nerve stimulation Treatment: Pyridostigmine (inhibits Ach esterase) and immunosuppressive (steroids, IVIG)

Answer 6

Stroke is defined as an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology. Further subdivided into **ischaemic stroke** (caused by vascular occlusion or stenosis) and **haemorrhagic stroke** (caused by vascular rupture, resulting in intraparenchymal and/or subarachnoid haemorrhage) 3rd leading cause of death and major cause of disability **Causes**: AF, Athersclerosis, AV malformation **Differentials**: Migraine, Seizure, Hypoglycaemia, tumour, syncope **Pathophysiology:** - Vessel occlusion due to thrombus from athersclerosis or embolism from carotid a./aorta) - Reduced cerebral blood flow - Cell death due to exitoxicity, peri-infart, oxidative stress, depolarisation, inflammation, apoptosis - Leads to ischaemia (reduced blood flow) and eventually infarction (irreversible damage due to reduced flow) **Transient ischaemic attack (TIA):** transient episode of neurological dysfucntion caused by focal ischaemia, without infarction. High risk of ischaemic stroke.

Answer 7

**Clinical presesntation:** Weakness in on side of face/arms/legs (hemiparesis) Dysphasia (impaired language) Visual disturbance Acute light headedness (past-pointing (when pointing at object, will point too far), nystagmus) **Investigations:** FBC, UE, CRP, LFT, lipid profile, glucose, coagulation profile Glucose, platelet count, coagulation profile may influence acute management ECG (ischaemic changes, AF) CT (differentiate between ischaemic/haemorrhagic, exclude tumor) CT angiogram/MR angiogram (identify site of thrombus, identify ischaemia penumbra - ischaemic tissue that is at risk of infarction but potentially savalgable if reperfusion occurs quickly) **Management:** **Ischaemic stroke:** IV thrombolysis (within 4.5 hours) - Alteplase - NNT: 3.1 Trombectomy (within 6-8 hours) (surgery to remove blood clot) Aspirin Admitted to Stroke Unit Hemicranectomy **Haemorrahagic stroke:** BP control Admitted to Stroke Unit Neurosurgical evaluation **Secondary prevention:** Statins, Antiplatelets (clopidorgel or aspirin), antihypertensive e.g. ACEi Physio, OT, Speech therapy

Answer 8

Genetics Poverty Smoking Alcohol Obesity Hypertension Common secondary prevention: Stop smoking, less drinking, lose weight, statins, aspirin

Answer 9

Defintion: Focal collection of blood in brain parenchyma or ventricular system not due to trauma Causes: - Small vessel disease - Blood clotting disorders - Tumours - Drugs e.g. cocaine

Answer 10

**TACS (total anterior circulation syndrome)** - higher cortical dysfunction (dysphasia, visuospatial disturbances), hemiparesis+hemianopia - MCA (middle cerebral a. or internal carotid a.) **PACS (partial anterior circulation syndrome)** isolated higher cortical dysfunction or 2 of cortical dysfucntion, hemianoipia, hemiparesis - branch MCA **POCS (posterior circulation syndrome)** - isolated homonymous hemianopia, brainstem syndrome (e.g. nystagmus, cerebellar signs), cranial nerve pasly (ipsilteral) with contralateral motor/sensory defect, bilateral motor/sensory, - PCA, cerebellar arteries **LACS (lacunar syndrome)** - pure motor (hemiparesis) or sensory stroke or ataxic (lack of voluntary movements) hemiparesis, dysarthria, clumsy hand, mixed sensorimotor - perforating artery, small vessel disease

Answer 11

**Numbness and weakness in face/arms/legs** Numbness:primary somatosensory cortex becomes damaged Weakness - primary motor cortex becomes damaged Ant cerebral a. - motor/sensory symptoms in legs Middle cerebral a. - symptoms affecting face/upper limbs Damage to one side will affect body on other side **Dysphasia (difficulty speaking)** Left hemisphere (dominant hemisphere) Middle cerebral a. supplies Broca's area (fluid speech production), Wernicke's area (understanding speech) **Visual disturbances** Posterior cerbral a. Homonymous hemianopia **Acute lightheadedness** Stroke in cerebellium (past-pointing (when pointing at object, will point too far), nystagmus)

Answer 12

**Definition:** Acute cerebrovascular event where there is bleeding into the subarachnoid space and is an emergency **Clinical presentation:** Sudden onset headache (worst in their life), nausea/vomiting, loss of consiousness, visual/speech disturbances, seizures Clinical examination: Photophobia, meningism, vitreous haemorrhage of eye (Terson's syndrome), speech and limb disturbance **Causes:** Trauma (most common) Saccular/Berry aneurysms (bulge of intimal layer through muscular wall of a. due to weakened muscular layer of blood vessel wall) - most common cause of non-traumatic SAH - Most aneursyms at bifurcation of ant. communicating and ant. cerebral a. or ICA and post. communicating a. - AV malformation, neoplasm, polycystic kidney disease, Ehlers Danlos syndrome **Pathogenesis**: Aneurysm forms due to increased haemodynamic stress which leads to inflammatory and immunlogical reactions and vascular remodelling **Predisposing factors:** Smoking, Female, Hypertension, Ehlers Danlos Syndrome Graded by WFNS Grades I-V: GCS (lower GCS, higher grade) Those with non-traumatic SAH, and no aneurysm - perimesencephalic SAH

Answer 13

**Investigations:** **CT:** confirms diagnosis, identifies complications e.g. infarction, hydrocephalus, Fisher Grade used to CT scans for prognosis **Lumbar puncture**: xanthochromia (bilirubin in CSF (cerebrospinal fluid) Once confirmed with CT or LP, causative aneursym can be found using: **CTA** (CT angiography - contrast injected to highlight arterial vasculature) **DSA** (digital subtraction angiography) - contra-indicated in diabetics, strokes Hyponatraemia ECG Troponin levels **Management:** Bed rest Fluids - normal saline Analgeisa IV **Nimodipine**: Ca2+ antagonist (prevent vasospams which causes cerebral ischaemia) Surigcal clipping (close base of aneurysm with a clip) Endovascular coils (platinum coil inserted into aneurysm, and blodo clot forms around platinum coils which seal aneurysm off.

Answer 14

Reharmorrhage (clipping or coiling need to be peformed) Vasospasm (nimodipine used to prevent it) Hydrocephalus (accumulation of CSF in brain) Delayed Ischaemia Hyponatraemia Cardiopulmonary complications e.g. arrythmias Seizures (can be treated with phenytoin) Predictors of poorer outcome: focal neurological deficit, reduced GCS at presentation, development of complications

Answer 15

Primary headache: Headache and assoc. features is primary disorder e.g. migraine, tension, cluster Secondary headache: Headache is due to underlying disorder e.g. SAH, space-occupying lesion, temporal arteritis, meningitis Red flags features suggesting secondary headache: Systemic symptoms e.g. fever, weight loss Neuroligcal deficit Onset is acute (thunderclap headache) Older age onset (\>50yrs) Triggered by posture, valsalva (coughing/straining) - indicates high/low CSF pressure headaches

Answer 16

Onset - time to maximal symptoms, what happened around onset Severity pain - scale, description Location Aura Timing - duration, frequency Other symptoms: photophobia, nausea, vomiting (common in migraine) Age of onset: Childhood (migraine), \>50 yrs (secondary) Triggers e.g. valsalva Family history (migraine strong FH) Social history Medication

Answer 17

Mostly no abnormal signs, abnormal signs suggest secondary cause General exam: Concious level, BP, pyrexia, meningism Cranial nerve exam: Pupillary responses, visual fields, eye movements, fundoscopy Upper motor neuron signs: Pronator drift, increased tone, extensor plantar repsonse Cerebellar signs: Nystagmus (involuntary eye movements)

Answer 18

**Site:** Unilateral **Onset:** Gradual (may have aura before) Aura may be postive (flickering lights) or negative (visual loss) **Character:** Throbbing **Radiation:** Generalised **Assoc. Symptoms:** Photophobia, nausea, vomiting. changes in speech, apetite **Timing:** hours-days **Exacerbating symptoms:** stress, alcohol, menstruation **Relieving factors:** lying in dark room **Severity:** Can be severe **Relevant factors:** female, young, OCP, family history, medication overuse headache - assoc. with NSAIDs **Pathophysiology:** Dysfunction in trigeminovasuclar system involving pain sensitive cranial blood vessels, trigeminal nerves which innervate them and cranial parasympathetic outflow. - Prodome:up to 48 hrs before headache, symptoms: mood disturbance - Aura: reversible focal neurological symptoms e.g. visual (scotoma - dark spot in visual field). Due to reduced bloof flow to hemispheric regions opposite to symptoms. **Management:** Analgesia Triptans e.g. Sumatriptan (5-HT1 agonist) Metoclopramide (anti-emetics) Prophylaxis: tricyclic antidepressants (amitriptyline) Advise pts on triggers Reduce caffiene, alcohol Encourage regular meals, good sleep pattern

Answer 19

**Definition:** sudden onset severe headache, reaches max intensity \< 5mins Considered as SAH until proven otherwise **Site:** Occipital **Character:**"hit on back of head" **Assoc symptoms:** **- Meningismus** (photophobia/neck stiffness/headache), vomiting, speech disturbance Signs: **Positive Kernig's sign** (hip and knee are flexed at 90 degrees, and pain elicited when knee is extended - suggets irritation of meninges) - Terson's syndrome, Pulmonary oedema **- IIIrd nerve palsy** ( eye down and out, with **dilation** of pupul - **surgical palsy**, as parasym fibres which supply pupillary constrictor muscles are **compressed** from "surgical causes" (from **aneurysm** - **posterior communicating a.**). IIrd nerve palsy with no dilation in diabetic pt - ischaemis of small vessels) Most common non-traumatic cauase: due to **berry aneurysms** (out pouching of intima through musclar wall) - Most commonly at anterior cerebral cirulation,. bifurcation of **anterior and anterior communicating** - **Internal carotid and posteior communicating** at **middle cerebral burification** **Relevant factors:** Usually due to aneurysm, more common in polycystic kidney disease, Ehlers Danlos Syndrome Risk factors: smoking, alcohol, hypertension **Causes:** SAH, intracerebral haemorrhage, bacterial meningitis, primary headache **Investigations** Bloods: FBC, U+Es, LFTs, glucose ECG - ischaemic changes can be seen CT - 90% pts will have blood in ventricles (appears white on scan) LP: xanthochromia (yellow discolouration of CSF due to bilirubin) - only peformed 12 hours after

Answer 20

Brain, blood, CSF 7-15 mmHg Monroe-Kellie Hypothesis: increase in one component, causes reduction in other two Cerebral perfusion pressure (CPP): pressure gradient causing blood flow to brain CPP = MAP - ICP When ICP increasesd, brain perfusion decreased Above 25mmHg intracranial volume can cause marked increase ICP **Signs of raised ICP:** Papilloedema Restricted visual field Enlarging blind spot Abducens nerve palsy may be false localising sign of raised ICP

Answer 21

History: Worse when lying flat, better when sitting/standing up Worse in morning, valsalva, physical exertion Persistent nausea/vomiting Examination findings: Optic disc swelling (papilloedma) Enlargment of blind spot Restricted visual field IIIrd, VIth (oculomotor or abducens) nerve palsy Causes: Tumour, hydrocephalus, meningitis

Answer 22

Worse when sitting/standing, better when lying down Causes: CSF leakage Post lumbar puncture Spontaneous intracranial hypotension - dural tear

Answer 23

**Cluster headache (trigeminal autonomic cephalgias)** - Site: Unilateral, around eye Onset: peaks within mins Assoc symptoms: red eye, lacrimation, nasal congestion, ptosis+miosis (constricted pupil) Timing: around 30 mins, usually same time each day Relevant factors: more in men, heavy smoking/alcohol **Tension headache:** Site: Bilateral Onset: gradual Character: tight band aorund head Assoc symptoms: none **Idiopathic intracranial hypertension:** Site: generalised Assoc symptoms: visual changes, papilloedema on fundoscopy Exacerbated by lying down Better than standing up

Answer 24

SAH Intracerebral haemorrhage Bacterial meningitis

Answer 25

Seizure: episode of neuronal hyperactivity Epilepsy: at least 2 unprovoked episodes of seizure

Answer 26

Seizures are either generalised (starts on one point but rapidly spreads bilaterally) or focal (partial) - limited to on area but lead to a generalised seizure **Focal:** History trauma Focal aura Post-attack confusion Automatisms (unconcious movements e.g. picking at clothes) Nocturnal events **Generalised:** Young No aura Photosensitivty Myoclonus (jerky movements) - esp. in morning Seizures within 2hrs of awakening Positive family history EEG abnormal

Answer 27

MRI, EEG, systemic provocation

Answer 28

Syncope NEAD (non-epileptic attack disorder) Migraine Narcolepsy Panic attacks

Answer 29

More than 2 seizures without full recovery, or neurologic function between seizures or Contiuous seizures more than 30 mins - Medical emergency, can cause profound neurlogical damage Management: Phenytoin, Gabapentin, Pregabalin

Answer 30

**Focal epilepsy:** Lamotrigine, Carbamazepine, Levetiracetam **Generalised epilepsy:** Sodium Valproate, Levetiracetam, Lamotrigine Status epilepticus: **Phenytoin, Gabapentin, Pregabalin** **Carbamezepine** (inhibits voltage gated Na+ channel on pre-synaptic membrane, decreased neuronal excitability, decreasing AP transmission) SE: headache, hyponatraemia, SJS **Lamotrigine** (inhibits voltage gates Ca+ and Na+ channels on pre-synaptic membrane) SE: Insomnia, SJS **Levetiracetam** (inhibits SV2A (synaptic vesicle) decreasing NT release) SE: headache, faitgue, anxiety **Sodium valproate** (weak Na channel blocker. Increases GABA by decreasing GABA degrading enzymes, leading to neuronal inhibition SE: hyponatraemia, SJS **Phenytoin** (Inhibits voltage gated Na+ channel on pre-synaptic membrane, decreasing AP transmission) SE: headache, insomnia, SJS **Gabapentin, pregabalin** (inhibits voltage gated Ca+ channel)

Answer 31

Meningitis - infection of meninges (Bacteria, viral) Encephalitis - infection of brain itself (Viral, bacterial) Mass lesion - abscess Myelitis - infection of SC (staph. aureus or viral (CMV))

Answer 32

Bacterial: Meningitis Meningococcus, pneumococcus, haemophilus influenzae Viral: Encephalitis Enterovirus, HSV, VZV Fungal: Meningo-encephalitis Cryptococcosis Protazoal: Mass lesion Toxoplasmosis

Answer 33

Inflammation of meninges +/- cerebrum Acute: bacterial or viral (viral more common, but bacterial more severe) Sub-acute: Bacterial (listeria (more common in elderly) or TB) Most common: neisseria meningitidis, strep. pneumoniae,

Answer 34

95% will have 2 of: Headache, neck stiffness, reduced GCS or fever Confusion suggests encephalitis Rash - pupuric (non-blanching) or petechial, but macular early on (meningococcal) Complications: Hydrocephalus, hearing loss, seizures

Answer 35

**Pneumococcal:** - Middle ear disease - Head injury - Alcohol - Immunosuppression Listeria (through unpasterised foods e.g. pate) - Immunosuppression - Pregnancy

Answer 36

Neurological complications e.g. CN palsies (CN VIII palsy - hearing loss), focal neurological signs, seizures Pneumococcal infection usually multi-focal. Can have pneumonia, endocarditis as well Splenectomised pts more at risk, require pneumococcal vaccination or antibiotic prophylaxis

Answer 37

Adverse outcome: Pneumococcus Reduced GCS Age CN palsy (pneumococcal) Bleeding (meningococcal)

Answer 38

History and exam - examine throat and cervical lymph nodes Blood cultures (blood PCR) Bloods - FBC, U&Es, LFTs, CRP Throat culture LP: - gram stain, culture, PCR - protein and glucose bacterial meningitis - low glucose, high protein, high lactate CT - to exclude mass lesion, cerebral oedema (doesn't exclude raised ICP) Antibiotics given before scan CT before LP if: - GCS \<12 - CNS signs - Seizures - Papilloedema - Immunocompromised

Answer 39

Brain shift Rapidly reduced GCS Severe sepsis Infection at LP site Coagulopathy

Answer 40

**Bacterial:** Cells: Neutrophils Lymphocytes (listeria) Glucose: \< 50% of blood glucose Protein: High Other: culture, PCR **Viral:** Cells: lymphocytes Glucose: Normal Protein: Raised Other: PCR **TB** Cells: lymphocytes Glucose: \<50% Protein: Raised Other: PCR **Fungal**: Cells: lymphocytes Glucose: \<50% Protein: High Other: India ink (shows cryptococcal)

Answer 41

**IV Ceftriaxone** If immunocompromised or listeria suspected: ADD **IV amoxicillin** If BM strongly suspected: ADD **IV dexamethasone**

Answer 42

Meningococcus: **IV Ceftriaxone** 5 days Pneumococcus: I**V Ceftriaxone** 14 days Listeria: **IV Amoxicillin** 21 days - Can give corticosteroids with suspected BM - Give close secondary contacts prophylaxis e.g. Ciprofloxacin, Rifampicin

Answer 43

Diagnosed after excluding bacterial No confusion Aetiology: Enterovirus \> HSV 2\> VZV \> HSV 1 Supportive treatment Aciclovir if immunocompromised

Answer 44

Confusion, fever, seizures **Usually HSV** Investigations: CSF - lymphocytic, normal glucose EEG - abnormal acitivity in temporal lobe MRI Treatment: Aciclovir

Answer 45

Sub-acute (weeks) Can be found druing TB treatment CN leisions - CN III, IV, VI, IX (oculomotor, trochlear, abducens, glossopharyngeal) Usually paradoxical worsening Treatment: RIPE and steroids

Answer 46

Autoimmune destruction of CNS myelin and oligodendrocytes, characterised by 2 episodes of neurlogical dysfunction separated by time and space HLA-DR2 Demylination causes loss of neurological function: - Weak leg - Visual loss - nystagmus, optic neuritis - Urinary incontinence Deficits develop gradually, lasts more than 24 hrs and gradually improves Types: Relapsing remitting (unpredictable attacks followed by remission) - 70% Primary progressive (steady decline) - 10% Secondary progressive (starts as relapsing remitting, but then declines with no remission) Benign MS (mild attacks, long periods no symptoms) **Differentials:** Sjogren's syndrome, CNS vasculitis, Behcet's disease

Answer 47

**Optic neuritis** - inflammation of optic nerve - Painful loss of vision **Transverse myelitis** - inflammtion of SC Weakness, sensory loss, incontinence **Clinically isolated syndromes** - single episodes of neurological disability due to focal inflammation of CNS - Can include optic neuritis and transverse myelitis - May be first attack of MS **Radiologically isolated syndromes** MRI findings that look like MS but no signs/symptoms

Answer 48

**Diagnosis:** Clinical diagnosis based on history, supported by examinational and investigations 2 or more evidence of demylination disseminated in time and space **Investigations:** MRI brain and cervical spine with gadolinium contrast - Demyelination in 2 areas - indicates dissemination in space McDonald criteria: - periventricular, juxtacortical, infratentorial (e.g. cerebellum), SC - Enhanced and non-enhanced areas (suggests lesions of different ages) - indicates dissemination in time LP: - **CSF oligoclonal bands** (immunoglobulin bands after protein electrophoresis. Bands in CSF but not blood suggests immunoglobulin production in CSF) - cell counts - glucose - protein Bloods - exclude other conditions FBC, B12/Folate, ESR/CRP. LFTs, aquaporin-4 antibody (marker of optic neuritis, transverse myelitis) **Visual evoked potentials** (measures speed of impulses travelling along optic nerve. Conduction slower in optic neuritis) CXR exlcude sarcoidosis

Answer 49

Unknown, multi-factorial: Genetic factors Low sunlight/vitamin D exposure Viral - EBV Smoking

Answer 50

Visual: optic neuritis (manifests as opic disc pallor - optic atrophy, relative afferent pupillary defect), dipoplia. internuclear opthalmoplegia Speech: dysarthria Muscle: weakness, spasms Central: fatigue Incontinence, diarrhoea/constipation Uthoff's syndrome - symptoms worse with heat Signs: Hoffman's sign (UMN sisgn) - flick nail of middle figer and ipsilteral thumb flexes - positive

Answer 51

Sudden onset Major cognitive involvement Pyrexial/Evidence of infection Normal MRI

Answer 52

Relapse: involves new neurological deficit that lasts more than 24 hrs, absence of infection Pseudo-relapse: previous neurological symptoms re-emerge Treatment: Not all relapses need treatment Steroids (not to be given if evidence of infection) - IV Methylprednisolone (3 days) or oral methylprednisolone (5 days) and PPI (gastroprotection)

Answer 53

Increased tone Spastic Muscle weakness Hyper-reflexia Clonus Entensor plantar (abnormal) Postive Hoffman's sign

Answer 54

Progressive multifocal leukoencelopathy Sarcoidosis Lyme disease Sjorgen's syndrome

Answer 55

**Relapsing-remitting MS** 1st line: **Dimethy fumerate** (supresses immune system) Risks: GI side effects 2nd line: **Fingolimod**: Risks: brain infections Disease modifying dugs: **Natalizumab:** - Risk of PML if infected with JC virus 3rd line: **Alemtuzumab** - Risk of secondary autoimmune disorders e.g. thyroid Escalating therapy: start with weaker treatments, work up Induction therapy: starts with stronger treatments (Alemtuzumab) Physio, OT **Primary progressive MS** Currently no disease modifying therapies Symptom control e.g. Modafinil for fatigue, tamsulosin for urinary symptoms, gabapentin for spasticity

Answer 56

Progressive cognitive decline - Inteferes with ability to function at work/daily activities - Not explained by delirium or major psychiatric disorder Needs to involve more than one brain region: Memory (temporal) Executive function (frontal) Language (temporal) Apraxia/visuospatial (parietal)

Answer 57

MMSE Addenbrookes cognitive assessment (examines memory, attention, language, visuospatial, executive function) Memory - tests by recall, anterograde memory (give them a name and get them to repeat, and ask again later), retrograde memory (ask about historical famous people) Attenttion - filtering information to focus on one stimuli. Testing by orientation, serial 7s However, bedside testing limited to episiodic and semantic memory Addenbrooks (ACEr): cut-off score 88 or 83

Answer 58

Starts in temporal lobe and spreads to frontal and parietal Mild stage: episodic memory Moderate stage: visuo-spatial Severe stage: language Excess amyloid precursor protein being broken down into beta amyloid deposits leading to formation of plaques. Leads to inflammatory process causing neuronal death

Answer 59

Frontal lobe Behaviour/social awareness (orbitofrontal) Working memory (dorsolateral pre-frontal cortex) Motivation (anterior cingulate) Tests: verbal fluency, proverbs

Answer 60

Parietal lobe Accurately localise objects Tests: Drawing pentagons, cubes

Answer 61

Disorders: Progressive non-fluent aphasia Tests: Repitition, reading

Answer 62

Loss of: Episodic memory - AD semantic memory - semantic dementia (loss of knowledge about world inc. words. Teted by reading irregular words. Attention: Delirium Naming: Progressive non-fluent aphasia Visuospatial: PD plus syndrome

Answer 63

6% cases are monogenic causes e.g. PARK8 (encodes LRRK2 protein) Pathology: Loss of dopaminergic neurons in SN. Remaining neurons have Lewy bodies. PD manifests when there is loss of 50% dopmainergic neurons Lewy bodies: a-synucelin, ubiquitin. Formed due to oxidative stress, exitoxicity, inflammation Pathological progression Stage 1 - 2: ant. olfactory nucleus, medulla/pons - presymptomatic/pre-motor PD e.g. loss of smell Stage 3-4: SN in midbrain - PD Stage 5-6: neocortex - PD dementia

Answer 64

Bradykinesia (slowness in initiating voluntary movements, progressive reduction in speed of repetitive actions) And at least one of: - Muscular rigidity - Rest tremor - Postural instability Non-motor symptoms: Cognitive: Dementia Autonomic: constipation, postural hypotension Fatigue

Answer 65

Essential tremor Demential with Lewy bodies Parkinson plus disoders Drug induced Parkinsonism

Answer 66

Bloods (if tremor present - thyroid function tests, copper (Wilson's disease) CT/MRI - normal in PD - abnormal in vascular parkinsonism Functional imaging - DAT-SPECT (image presynaptic dopaminergic function) abnormal

Answer 67

Clinical aim: imrpove motor symptoms, QOL **L-DOPA** Taken up by dopaminergic neurons and decaroxylated to dopamine in presynaptic terminals. Striatal dopaminergic neurotransmission increased. + dopamine decarboxylase inhibitor (**carbidopa**, benserazide) - to reduce being converted in periphery Adverse effects: nausea, vomiting, postural hypotension, hallucinations, dyskinsia **Dopamine agonists:** **Apomorphine** Sitmulates post-synaptic striatal dopamine receptors (D2) Longer half life than L-dopa, fewer motor complications Adverse effects: nightmares, impulse control disorders e.g. pathological gambling MAO-inhibitors: **Selegelline** Prevents dopamine breakdown by inhibiting enzyme, monoamine oxidase COMT-inhibitors: **Entacapone** Co-pescribed with L-dopa Inhibits COMT, prevents peripheral breakdown of levodopa so more reaches the brain SE: dyskinesia, nausea, vomiting

Answer 68

GP Neurologist Physio OT SALT

Answer 69

Degenerative: Dementia with Lewy bodies Secondary: Drug induced parkinsonism (e.g. chronic use of dopaminergic antagonists) Cerebrovasuclar disease Toxins (e.g. MPTP)

Answer 70

Posture and voluntary movement Input:cortex Output: cortex and brainstem Basal ganglia loops Motor: movement Eye movement: oculomotor Lateral - orbito frontal: social behaviour Dorsolateral prefrontal cortex: working memory, executive function

Answer 71

Tumour Hydrocephalus Meningitis Idiopathic intracranial hypertension

Answer 72

Perimesencephalic SAH

Answer 73

Upper motor neuron: Increased tone Pronator drift Extensor plantar reflex Cerebellar signs: Nystagmus Past pointing Dysdiadochokinesis (inability to peform repeating, alternating movements) Broad-based ataxic gait

Answer 74

Antiplatelets e.g. aspirin (if had thrombolytic therapy, should not have it until 24 hrs after, and not until CT has excluded haemorrhage) Statins ACEi and thiazide (aim below 140/80) Physio, OT, speech therapy

Answer 75

VZV infection of facial nerve Complication of shingles Facial palsy and hearing loss Vesicles on auditory canal, soft palate

Week 12 Neuro Flashcards

(99 cards)