Neurology Flashcards

Question

Explain the aetiology/risk factors of migraine?

Answer 1

Brain hyperexcitability to various stimuli Neuronal depolarisation is believed to be the precipitating event in migraine aura ``` Risk factors: Family history of migraines High caffeine intake Exposure to change in barometric pressure (altitude and weather changes) Female Obesity Habitual snoring Stress Overuse of headache medication Lack of sleep OCP Allergies or asthma Hypertension Hypothyroidism Diet (alcohol, cheese, chocolate) ```

Answer 2

High prevalence - 14% of individuals More likely in females (3:1 F:M) Prevalence rises in early adult years then decreases in late 40s-50s More common in white patients Highest amongst low income patients Highest in Americas and Europe, lowest in Asia

Answer 3

Prolonged headache - 4-72 hours, may be throbbing Nausea/vomiting Decreased ability to function Sensitivity to light Headache made worse by activity - distinguish between migraine and tension headache (tension not worsened by exertion) Sensitivity to noise Aura: Visual disturbances (Flashing lights, Spots, Blurring, Zigzag lines, Blind Spots), Other sensory symptoms (tingling or numbness in limbs)

Answer 4

Nil signs of note

Answer 5

Mainly a clinical diagnosis from the history Investigations to rule out other causes: ESR - if raised, suggests temporal arteritis Lumbar puncture - if abnormal could be SAH, meningitis or low or high cerebrospinal fluid pressure CSF culture - if CNS infection CT head/MRI brain - may show space-occupying lesion, ischaemic lesions, SAH

Answer 6

Acute with persistent symptoms: paracetamol, codeine, anti-emetics, triptans (5-HT agonists) eg sumatriptan, high flow oxygen, IV corticosteroid (NSAIDs) Prophylaxis (if > 2 months): β-blockers, Amitriptyline, Topiramate, Sodium Valproate (tricyclic antidepressants, anticonvulsants) Menstrual migraines can be controlled with the oral contraceptive pill ``` Advice: Encourage Regular meals and Sleep Caffeine Restriction Measures to Reduce Stress Symptom Diary Avoid triggers Rest in quiet, dark room during episodes ```

Answer 7

Disruption of daily activities Can progress into analgesia-overuse headaches in people who use analgesia regularly Status migrainosus - migraine occurring for more than 72 hours Migranous infarction - occurs when an aura lasts more than 1 hour Migraine-triggered seizures Depression Chronic migraine - 15 or more days per month for more than three months with no medication overuse Persistent aura without infarction

Answer 8

Patients do well with treatment The frequency of migraines decreases with age Usually chronic

Answer 9

Sudden onset of neurological signs and symptoms caused by focal brain, spinal cord or retinal ischaemia (temporary occlusion of part of cerebral circulation) without acute infarction which resolves completely within 24 hours.

Answer 10

Most common cause = carotid artery stenosis Cardioembolic events: Carotid atherosclerosis Emboli can arise from the heart: AF, atrial myxoma, mitral valve disease Small vessel occlusion: microatheromas, fibrinoid necrosis Others: occlusion due to hypercoagubility, dissection, vasculitis, vasospasm

Answer 11

``` HYPERTENSION AF Coronary Artery Disease Diabetes Increasing age Male Obesity Hypercholesterolaemia Family history Valvular disease Smoking Alcohol ```

Answer 12

2000 people per year in England have first TIA Prevalence increases with age More common in men Less common in white patients

Answer 13

Clinical features depend on the part of the brain affected: Carotid Territory: Unilateral Affect the MOTOR AREA Weakness of arm, leg or one side of the face Dysarthria Broca's dysphasia Amaurosis fugax (painless fleeting loss of vision caused by retinal ischaemia) ``` Vertebrobasilar Territory: Homonymous hemianopia (if ophthalmic cortex is involved) Bilateral visual impairment Hemiparesis Hemisensory symptoms Diplopia Vertigo Vomiting Dysarthria Dysphagia Ataxia ```

Answer 14

Neurological examination may be NORMAL because the TIA may have resolved Check pulse for irregularly irregular rhythm (AF) Carotid bruit (carotid atherosclerosis) Elevated BP (rises acutely after a cerebral ischaemic effect by increasing cerebral blood flow)

Answer 15

Bloods: Glucose - hypoglycaemia can cause similar symptoms FBC ECG - check for AF MRI brain - may show infarct Carotid doppler ultrasound if expecting carotid stenosis MR/CT angiography to further investigate carotid stenoses Echo - check for valvular disease

Answer 16

Patient presenting with suspected TIA = 300mg aspirin immediately and assess urgently within 24 hours Patients with confirmed TIA should receive: Clopidogrel: 300 mg loading dose and 75 mg thereafter High-Intensity Statin Therapy: e.g. atorvastatin 20-80 mg ``` Secondary Prevention: ANTI-PLATELETS EG ASPIRIN ANTIHYPERTENSIVES (hypertension is biggest RF) Lipid-modifying treatments Management of AF Life style modification ``` Carotid endarterectomy (artery opened and clot removed) IF: >70% stenosis Symptomatic TIA or good recovery stroke in past 6 months involving anterior cirulation Assessment of future stroke risk in TIA patients: ABCD2 score Age >60 Blood pressure - systolic >140mmHg Clinical - unilateral weakness (2), speech deficit (1) Duration of symptoms - >60mins (2), 10-59mins (1) Diabetes ``` 0-3 = 1% 2 day stroke risk 4-5 = 4.1% risk 6-7 = 8.1% ```

Answer 17

Recurrent TIA Stroke MI

Answer 18

>10% seen in A&E will have stroke within 3 months

Answer 19

An acute unilateral, idiopathic facial nerve palsy, likely of viral aetiology. It is a peripheral/LMN lesion.

Answer 20

It is idiopathic Likely a viral aetiology - most likely HERPES SIMPLEX VIRUS May be EBV or Varicella Zoster 60% are preceded by an upper respiratory tract infection

Answer 21

``` Intranasal influenza vaccination Pregnancy (3 times more common) Upper Respiratory Tract Infection Family history Diabetes Hypertension ```

Answer 22

Most common aetiology of unilateral facial palsy Most prevalent between 15-45y/o Equal distribution between both sexes

Answer 23

``` Preceding ear pain (1-2 days before) Rapid onset symptoms Unilateral facial muscle weakness/paralysis Drooping eyelid and mouth Dry mouth and eyes Difficulty closing eye Loss of taste sensation Phonophobia Speech impairment Drooling saliva ```

Answer 24

LMN weakness of facial muscles: Affects IPSILATERAL muscles of facial expression Does NOT spare the muscles of upper part of the face (unlike UMN facial nerve palsy) Bell's Phenomenon - Eyeball rolls up but the eye remains open when trying to close their eyes Clinical testing of sensation is NORMAL Examine the ears to check for other causes of facial nerve palsy (e.g. otitis media, herpes zoster infection) BELL'S PALSY IS DIAGNOSIS OF EXCLUSION

Answer 25

Mainly a CLINICAL DIAGNOSIS - acute unilateral facial weakness with normal physical exam Viral serology Nerve conduction studies if palsy consists to rule out axonal degeneration EMG: may show absence of voluntary motor unit potentials Serology for Borrelia Burgdorferi: indicated in patients with travel to Lyme Disease endemic area

Answer 26

ALL PATIENTS: Protection of cornea with protective glasses/patches or artificial tears High-dose corticosteroids within 72 hrs i.e. short dose oral prednisolone Adjuncts: Concurrent Antiviral Therapy Encourage closure of eyelids by hand or tape at night Surgical decompression - lateral tarsorrhaphy (suturing the lateral parts of the eyelids together) – performed if imminent or established corneal damage

Answer 27

``` Corneal ulcers Dry Eyes Eye Infection Aberrant reinnervation (synkinesis) Gustatory Hyper lacrimation (PNS fibres may aberrantly reinnervate the lacrimal glands causing tearing whilst salivating) ```

Answer 28

Extent of facial palsy within 72 hours is predictive of recovery outcome 94% with incomplete paralysis will recover, 61% with complete paralysis will recover Pregnancy-associated Bell's palsy has worse outcomes Recovery within 2-12 weeks

Answer 29

An acute segmental demyelinating disease of the peripheral nervous system ACUTE INFLAMMATORY DEMYELINATING POLYNEUROPATHY

Answer 30

Cause unknown Immune mediated attack where antibodies formed after a recent infection react with self-antigens on myelin sheath or Schwann cells Often develops post: Bacterial infection - campylobacter jejuni, mycoplasma pneumoniae Viral infection - CMV, EBV Preceded by gastroenteritis or flu like symptoms within 6 weeks of symptoms Rarely triggered following influenza vaccination

Answer 31

Previous viral illness Bacterial infection Hepatitis E Mosquito-borne viral infection

Answer 32

Slightly more common in males Mean age of presentation is 40 Affects all age groups

Answer 33

Progressive symptoms Initially ascending symmetrical paresthesia - loss of vibration and touch sensation Ascending symmetrical muscle weakness/paralysis (more in upper limb and more proximal) Cranial nerve involvement - dysphagia, dysarthria, facial weakness, diplopia, difficulty speaking Respiratory muscles may be affected in SEVERE cases -dyspnoea on exertion & SOB Autonomic nerve involvement - palpitations, constipation, urinary incontinence

Answer 34

Hypotonia Flaccid paralysis Areflexia/hyporeflexia (ascending upwards from feet to head - notice loss of ankle reflex first) Impairment of sensation in multiple modalities (ascending from feet to head) Facial nerve weakness - slurred speech Abnormality of external ocular movements due to extra-ocular muscle weakness Type II Respiratory Failure due to paralysis of respiratory muscles: CO2 retention flap Bounding pulse Autonomic Function: Orthostatic hypotension BP fluctuations Arrhythmia

Answer 35

Lumbar puncture - high CSF protein/albumin with normal WBC and glucose (ALBUMINOCYTOLOGIC DISSOCIATION) Nerve conduction tests - reduced conduction velocity Pulmonary function tests (spirometry) - reduced FVC suggests ventilator weakness Bloods: LFTs (may be elevated), Anti-ganglioside antibodies in Miller-Fisher variant ECG: Arrhythmias may develop

Answer 36

A neuropathic facial pain syndrome in the distribution of one or more branches of the trigeminal nerve.

Answer 37

Associated with trigeminal nerve root compression at the root entry zone by a vascular loop - often by SUPERIOR CEREBELLAR ARTERY Systemic causes: MS Expanding cranial tumour

Answer 38

Increased Age Multiple sclerosis Female Hypertension

Answer 39

More common in feamles Peak 50-60 years old 4-13 per 100,000 Prevalence increases with age

Answer 40

Paroxysms of sudden, sharp, shooting, UNILATERAL facial pain lasting less than 2 minutes Pain lasts from seconds to 2 minutes Pain is in trigeminal distribution Pain bought on by brushing teeth, chewing, shaving, breeze, touching area etc Recurrent & Periods of remission can vary Some experience preceding symptoms (e.g. numbness, tingling

Answer 41

MAY have sensory/motor changes - suggestive of pathological cause NO VISION LOSS NO ASSOCIATED NEUROLOGICAL DEFICIT

Answer 42

CLINICAL DIGANOSIS so usually no investigations If there is doubt over the underlying cause, specialists may request an: Intra-oral X-ray: if dental cause of pain is suspected MRI brain scan: if history or examination suggests other pathology Trigeminal Reflex Testing: abnormal reflexes suggestive of symptomatic trigeminal neuralgia

Answer 43

A chronic autoimmune condition affecting the post-synaptic membrane of neuromuscular junctions of skeletal muscles due to autoantibodies usually against nicotinic acetylcholine receptors. This causes muscle weakness and fatiguability.

Answer 44

Impairment on NMJ transmission Autoantibodies against nicotinic acetylcholine receptors on postsynaptic membrane at NMJ preventing muscle contraction - 80-90% of patients Minority of patients have muscle specific receptor tyrosine kinase anitbodies - 3-7% May present as paraneoplastic syndrome - associated with thymoma and bronchogenic carcinoma Associated with thymic follicular hyperplasia Associated with other AI conditions (e.g. pernicious anaemia) Lambert-Eaton Syndrome: paraneoplastic subtype of myasthenia gravis caused by autoantibodies against pre-synaptic calcium channels, leading to impairment of acetylcholine release

Answer 45

There is a bimodal distribution Young women aged 20-30 Older men aged 60-70 Affects women more than men MG with muscle-specific tyrosine kinase antibodies has 80-90% of patients as women. It is more common in black women and usually affects at mid-30s

Answer 46

Diplopia Ptosis Muscle weakness which worsens with repetitive movement or exercis - FATIGUABILITY Muscle weakness gets better on resting Usually wakes up fine Dysphagia Dysarthria Facial paresis Shortness of breath Disturbed, characteristic hyper nasal speech (dysarthria) Difficulty smiling, chewing or swallowing (nasal regurgitation of fluids)

Answer 47

May be generalised (affecting many muscle groups), bulbar or ocular Bilateral ptosis Complex ophthalmoplegia Check for ocular fatigue by asking the patient to sustain and upward gaze for 1 minute and watch the progressive ptosis that develops Reading aloud can provoke dysarthria or nasal speech Limbs: test power of muscle before & after repeated use (muscle fatiguability)

Answer 48

Serum acetylcholine receptor autoantibodies - positive in 80-90% of patients Muscle specific receptor tyrosine kinase antibodies TFTs (associated with hyperthyroidism) Anti-voltage gated Ca channel antibody (in Lambert-Eaton syndrome) Serial pulmonary function tests: indicated if patient has SOB & suspected MG crisis Repetitive nerve stimulation: reduced muscle action potential Single Fibre EMG CT Thorax/CXR: visualise thymoma (thymic enlargement) in mediastinum/lung malignancy NERVE CONDUCTION STUDY = GOLD STANDARD DIAGNOSTIC TEST

Answer 49

A syndrome caused by interruption of the sympathetic nerve supply to one side of the face, resulting in the triad of ptosis, miosis and anhydrosis.

Answer 50

Caused by disruption of the sympathetic nervous system supply to the face Damage to 1st order neurone: Tumour Syringomyelia Stroke Damage to 2nd order neurone: Apical lung tumour (pancoast tumour) Damage to 3rd order neurone: Internal carotid artery dissection Other: Neck trauma MS Lymphadenopathy

Answer 51

Rare | It is a sign associated with many conditions

Answer 52

``` Unable to open one eye fully Loss of sweating on affected side Facial flushing Orbital pain/headache Other symptoms based on CAUSE ```

Answer 53

Unilateral ptosis Unilateral anhidrosis Unilateral myosis Enopthalmos Symptoms are on ipsilateral side as lesion Can have decreased visual acuity and/or abnormal eye movement which warrants further investigation

Answer 54

Cocaine eye drop: Usually causes build up of NA by preventing reuptake which would cause dilation If no dilation - suggests Horner's Apraclonidine eye drop: Weaker form of cocaine which normally does not cause dilation If dilation of eye occurs - suggests Horner's CT/MRI - find underlying cause eg cerebrovascular accident CXR: apical lung tumour CT angiography: dissection

Answer 55

Depends on the underlying cause of Horner's | Surgical intervention is needed for syringomyelia, tumours, or carotid artery dissection

Answer 56

Hydrocephalus is enlargement of the ventricular system of the brain due to excessive build up of CSF. It can be communicating or non-communicating

Answer 57

Abnormal accumulation of CSF in the ventricles can be caused by: Impaired outflow of the CSF from the ventricular system: OBSTRUCTIVE Lesions of the 3rd and 4th ventricle or cerebral aqueduct Posterior fossa lesions (e.g. tumour) compressing the 4th ventricle Cerebral aqueduct stenosis Impaired CSF reabsorption into the subarachnoid villi: NON-OBSTRUCTIVE Tumours Meningitis Normal Pressure Hydrocephalus: idiopathic chronic ventricular enlargement. The long white matter tracts are damaged leading to gait and cognitive decline.

Answer 58

There is a bimodal age distribution Young: due to congenital malformations and brain tumours Elderly: due to strokes and tumours

Answer 59

Obstructive hydrocephalus: Diplopia Acute decrease in consciousness ``` Normal pressure hydrocephalus: Urinary incontinence Falls Abnormal walking Struggle to lift foot to initiate walking Memory loss Personality change Slow thought processing ```

Answer 60

Obstructive Hydrocephalus: Low GCS Papilledema 6th Nerve Palsy (6th nerve has the longest intracranial path of all the CN & so is most susceptible to palsy due to raised ICP) Normal Pressure Hydrocephalus: Cognitive impairment Gait apraxia (wide based, shuffling) Hyperreflexia Neonates: Increased head circumference and Sunset sign (↓ conjugate deviation of the eyes)

Answer 61

CT Head: 1st line for detecting hydrocephalus, may show cause (e.g. tumour). CSF: obtained from ventricular drain or lumbar puncture May indicate pathology (e.g. tuberculosis) Check MC&S, protein and glucose. Lumbar Puncture: CONTRAINDICIATED IF RAISED ICP as can cause tonsillar herniation & death. Therapeutic in normal pressure hydrocephalus.

Answer 62

Bleeding into the subarachnoid space (space between pia mater and arachnoid mater) and it is an emergency

Answer 63

``` Traumatic injury Saccular anuerysm rupture - main non-traumatic cause 80% Arteriovenous malformation Peri mesencephalic SAH Bleeding diathesis Vertebral artery dissection Use of anticoagulants ``` ``` Risk factors: Alcohol Smoking Family history Hypertension Autosomal dominant kidney disease Connective tissue disease eg Marfan's (predispose to aneurysm formation) ```

Answer 64

``` Incidence increases with age Average age of onset 50-55 years old More common in women More common in black patients Accounts for 5% of all strokes ```

Answer 65

``` Sudden onset, thunderclap, worst headache ever Photophobia Vomiting Neck stiffness Visual changes Confusion Seizures Reduced level of consciousness ```

Answer 66

Reduced consciousness Meningism: Neck stiffness, Kernig's sign, Pyrexia Signs of raised ICP - papilledema, IV or III nerve palsies, hypertension, bradycardia Focal neurological signs (e.g. cranial nerve palsies: CN III palsy indicates presence of posterior communicating artery aneurysm compressing CN III)

Answer 67

Non-contrast CT head - show bleeding (hyperdensity) within subarachnoid space, sensitivity decreases with time If CT normal but high suspicion - Lumbar puncture: Shows yellow xanthochromia. Must be performed more than 12 hours after onset. Take 3 tubes. FBC - leukocytosis Serum sodium - may be low Cerebral angiography can identify causal pathology CRP/ESR Clotting Profile (elevated INR, prolonged PTT) Cardiac Enzymes (troponin). ECG: Patients with SAH will have an abnormal ECG on admission i.e. arrythmias, prolonged AT, ST segment or T wave abnormalities.

Answer 68

An acute neurological, reversible emergency caused by thiamine (vit B1) deficiency, leading to a triad of confusion, ophthalmoplegia and ataxia which must be treated immediately to prevent chronic irreversible neurological changes.

Answer 69

Due to low thiamine causing CNS lesions Decreased thiamine intake - malnutrition, anorexia Decreased absorption - stomach cancer, IBD Chronic alcohol consumption Chronic alcohol consumption is the main cause: Liver cirrhosis prevents storage of thiamine Decreased absorption Prevents conversion to active form Inadequate nutritional thiamine intake ``` Other causes: Chronic subdural haematoma AIDS Hyperemesis Gravidarum Thyrotoxicosis ```

Answer 70

``` Alcohol Dependence AIDS Chemotherapy Malnutrition History of GI Surgery ```

Answer 71

Worldwide prevalence between 0.8-2.8% Prevalence higher in males Prevalence higher in patients with alcohol dependence, AIDS and bone marrow transplantation Higher prevalence in 50-60 year olds

Answer 72

Ophthalmoplegia - weakness of eye muscles Ataxia - unsteady gait and loss of muscle coordination Confusion Loss of consciousness Vision changes: diplopia, eye movement abnormalities, ptosis Loss of memory and Inability to form new memories Hallucinations Impaired concentration

Answer 73

TRIAD OF ATAXIA, OPHTHALMOPLEGIA AND CONFUSION Mental slowing, impaired concentration & apathy Ocular Motor Findings: gaze palsies, CNVI Palsy, Impaired Vestibulo-Ocular Reflex Papilledema, Retinal Haemorrhages Tachycardia AND/OR Hypotension Hypothermia or Hyperthermia Coma - decreased GCS

Answer 74

Diagnosis is mainly based on history and examination Serum thiamine - LOW FBC (high MCV is a common feature amongst alcoholics) U&Es (exclude metabolic imbalances as a cause of confusion) LFTs (elevated if due to chronic alcohol use) Glucose Blood alcohol level ABG (hypercapnia and hypoxia can cause confusion) Other: CT head, MRI Brain (show degeneration of mammillary bodies), Lumbar Puncture (exclude other pathology)