Neuro Flashcards

Question

Describe the complications for ischaemic stroke

Answer 1

Deep vein thrombosis, haemorrhagic transformation of ischaemic stroke

Answer 2

25% die within 1 year

Answer 3

Sudden onset, brief neurological deficit due to temporary, focal cerebral ischemia, without infarction. Last less than 24 hours, symptoms usually last 10-15mins.

Answer 4

Males, black people (predisposition to hypertension and atherosclerosis), 90% carotid artery (anterior circulation), 10% vertebral artery (posterior circulation)

Answer 5

Atherothromboembolism from carotid artery (main cause – listen for carotid bruit), cardioembolism (in atrial fibrillation, after MI, valve disease), hyperviscosity, hypoperfusion

Answer 6

Age, hypertension, smoking, diabetes, hyperlipidaemia, heart disease (AF), combined oral contraceptive pill, peripheral arterial disease, clotting disorder, vasculitis

Answer 7

Temporary, focal cerebral ischaemia causing lack of oxygen and nutrients to the brain, without infarction. No irreversible cell death.

Answer 8

Symptoms are maximal at onset, lasts 10-15mins. Amaurosis fugax (transient unilateral sudden vision loss due to retinal artery occlusion), aphasia (speech), hemiparesis (one-sided weakness/paralysis), hemisensory loss, hemianopia visual loss

Answer 9

Signs: ACA: weak, numb contralateral leg MCA: weak numb contralateral side of body, face drooping with forehead spared, aphasia PCA: vision loss (contralateral homonymous hemianopia with macular sparing) Vertebral: cerebellar syndrome (DANISH – dysdiadochokinesis (can’t perform rapid alternating movements), ataxia, nystagmus, intention tremor, slurred speech, hypotonia) Symptoms: Syncope, dizziness, ataxia, vertigo

Answer 10

Symptoms 10-15mins, <24 hours + no infarction

Answer 11

Bloods: FBC (look for polycythaemia), glucose, ESR (raised in vasculitis), U&Es, cholesterol, INR (if on warfarin), ECG, lipid profile, prothrombin time

Answer 12

Stroke, hypoglycaemia, migraine aura, focal epilepsy, vasculitis

Answer 13

1st line – immediate loading dose: aspirin 300mg (antiplatelet therapy). refer to specialist within 24hr of symptoms. Secondary prevention: clopidogrel 75mg daily (antiplatelet therapy), atorvastatin 80mg. Anticoagulation (e.g., warfarin) for atrial fibrillation patients. Carotid endarterectomy if >70% stenosis, reduces risk of TIA/stroke. Control CV risk factors: BP control, smoking cessation, statin, no driving for 1 month

Answer 14

ABCD2 risk of stroke after TIA (Age >60. BP. Clinical features: unilateral weakness, speech problems. Duration of TIA. Diabetes mellitus). FAST

Answer 15

Stroke, MI

Answer 16

Without intervention, 1/12 will have a stroke within a week

Answer 17

Type of haemorrhagic stroke. Spontaneous bleeding into subarachnoid space between arachnoid mater and pia mater. Can be catastrophic

Answer 18

Age 35-65. Black. Female. 5% of strokes.

Answer 19

Traumatic injury. Idiopathic Aneurysmal rupture – berry aneurysms (70-80% SAH causes, mc anterior communicating/ACA) Arteriovenous malformations (15% SAH causes) – abnormal tangles of blood vessels connecting arteries and veins.

Answer 20

Hypertension, known aneurysm, previous aneurysmal subarachnoid haemorrhage, smoking, alcohol, FHx, bleeding disorders. Associated with berry aneurysm: polycystic kidney disease, coarctation of aorta, Ehlers-Danlos and Marfan’s syndrome

Answer 21

Subarachnoid space contains circle of Willis arteries (ACA, MCA, PCA). * Tissue ischaemia: less blood can reach tissue due to bleeding loss, less oxygen and nutrients can reach tissue causing cell death. * Raised ICP: fast flowing arterial blood pumped into subarachnoid space * Space-occupying lesion puts pressure on brain * Blood irritates meninges causes inflammation of meninges (meningitis symptoms). Can obstruct CSF outflow – hydrocephalus * Vasospasm: bleeding irritates other vessels, ischaemic injury

Answer 22

Sudden onset excruciating headache (‘thunderclap’, typically occipital, worst headache of your life). Nausea, vomiting, collapse, loss of consciousness, neck stiffness. Sentinel headache (before main rupture)

Answer 23

Signs: Meninges inflammation: neck stiffness, muscle aches, Kernig sign (pain on passive extension of leg when the knee if flexed), Brudzinski sign (passive flexion of the neck causes hip and knee to flex) Retinal, subhyaloid and vitreous bleeds. Hypertension. Focal neurological signs, e.g., 3rd nerve palsy Symptoms: N+V, collapse, loss of consciousness, seizures, vision changes, photophobia, coma. Glasgow coma scale: eyes 4, verbal 5, motor 6. 3/15 = unresponsive. 8/15 = comatose. 15/15 = normal.

Answer 24

Urgent brain CT (subarachnoid and/or intraventricular blood, hyperattenuation in subarachnoid space, star shape sign)

Answer 25

1st line: Urgent brain CT (subarachnoid and/or intraventricular blood, star shape sign). If positive CT SAH > CT angiography. If negative CT SAH > lumbar puncture FBC (leucocytosis), U&E (hyponatraemia), clotting profile, glucose (raised), ECG (arrhythmias, prolonged QT, ST/T wave abnormalities) Other: Lumbar puncture: only if normal ICP to prevent coning. If -ve CT but strong suspicion of SAH. After 12 hours. Xanthochromia confirms SAH – yellowish CSF filled with breakdown products of RBCs MRI/CT angiography (establish source of bleeding)

Answer 26

Migraine, cluster headache, meningitis, intracerebral haemorrhage, carotid/vertebral artery dissection, arteriovenous malformation

Answer 27

Once SAH is confirmed, immediate neurosurgical referral (endovascular coiling or surgical clipping if aneurysm). IV fluids (maintain cerebral perfusion), Nimodipine (CCB – reduces vasospasm, reduces cerebral ischaemia)

Answer 28

Rebleeding, hyponatraemia, neuropsychiatric problems (mood change, memory loss), hydrocephalus

Answer 29

50% die straight away. 10-20% more die from rebleeding within weeks. Half the survivors are left with significant disability.

Answer 30

Bleeding into subdural space between dura mater and arachnoid mater due to rupture of a bridging vein

Answer 31

Babies (shaking baby syndrome), elderly, alcoholics

Answer 32

Head trauma, shearing deceleration injuries, dural metastases, brain atrophy, abused children (shaken baby syndrome)

Answer 33

Brain atrophy (veins more susceptible to rupture) – dementia, elderly, alcoholics. Epileptics. Anticoagulants.

Answer 34

Subdural space contains bridging veins which run from cortex to sinuses. Bleeding from bridging vein forms a haematoma (solid swelling of clotted blood), then bleeding stops. Weeks/months later, haematoma starts to autolyse causing a massive increase in oncotic and osmotic pressure. Water sucked in, haematoma enlarges. This causes a gradual rise in ICP. Midline strictures shifted away from side of clot > tentorial herniation, coning

Answer 35

Gradual onset with latent period. Headache, confusion, fluctuating consciousness, drowsiness, seizures. Signs of raised ICP: Cushing triad – bradycardia, increased pulse pressure, irregular breathing + fluctuating GCS.

Answer 36

Signs: Localising neurological signs: unequal pupils, hemiparesis, occur late often 1> month after injury Symptoms: Physical and intellectual slowing, personality change, memory loss, unsteadiness, headache, confusion, fluctuating consciousness, drowsiness

Answer 37

Brain CT scan (shows haematoma, crescent shaped banana – crosses suture lines, unilateral. Shows midline shift). Acute = hyperdense (bright blood) Subacute = isodense Chronic (late) = hypodense (darker than brain)

Answer 38

1st line: Brain CT scan (shows haematoma, crescent shaped banana – crosses suture lines, unilateral. Shows midline shift) Other: MRI scan

Answer 39

Epidural haematoma, intracerebral haematoma, stroke, seizure

Answer 40

Surgery – depending on clot size, chronicity, and clinical picture. Clot evacuation, Craniotomy, Burr hole washout. IV mannitol to reduce ICP. Reverse clotting abnormalities. Antiepileptics (phenytoin). Address cause of trauma.

Answer 41

Brainstem herniation, respiratory arrest, neurological deficits, coma, epilepsy

Answer 42

Bleeding into extradural space between dura mater and skull bone usually after trauma to temple

Answer 43

Young people, males

Answer 44

Trauma to temple – fracture to temporal/parietal bone, rupture of middle meningeal artery. Also due to dural venous sinus tear.

Answer 45

Head trauma, young people (as you age, dura is more firmly adhered to skull)

Answer 46

Extradural space contains middle meningeal artery After lucid interval, rapid rise in ICP causing pressure on brain, midline shift, tentorial herniation and coning.

Answer 47

Initial head trauma to temple/pterion. Short episode of drowsiness and unconsciousness. Lucid interval (can be hours-days). Then sudden, rapid deterioration. Rapidly declining GCS, increasingly severe headache, vomiting, seizures

Answer 48

Signs: Hemiparesis, UMN signs, ipsilateral pupil dilation, bilateral limb weakness, coma, deep irregular breathing due to coning (brainstem compression), bradycardia, raised BP. Symptoms: Headache, decreased consciousness, seizures, confusion, limb weakness

Answer 49

Brain CT scan (shows haematoma – biconvex lens-shaped lemon, doesn’t cross suture lines, hyperdense, unilateral. Shows midline drift.)

Answer 50

Brain CT scan (shows haematoma – biconvex lens-shaped lemon, doesn’t cross suture lines, hyperdense, unilateral. Shows midline drift.) Skull x-ray (fractures)

Answer 51

Subdural haematoma, intracranial haematoma, subarachnoid haemorrhage, migraine

Answer 52

1st line – urgent surgery (clot evacuation, ligation of bleeding vessel, burr hole craniotomy) IV mannitol to reduce ICP. Airway care (intubation, ventilation)

Answer 53

Brainstem compression, respiratory arrest, infection, cognitive impairment, death

Answer 54

15% mortality

Answer 55

Type of haemorrhagic stroke. Sudden bleeding into brain tissue due to rupture of a blood vessel within the brain

Answer 56

10% of strokes

Answer 57

Hypertension (stiff and brittle vessels, prone to rupture. Microaneurysms) Secondary to ischaemic stroke (bleeding after reperfusion) Head trauma, arteriovenous malformations, vasculitis, brain tumours, carotid artery dissection

Answer 58

Hypertension, age, alcohol, smoking, diabetes, anticoagulation, thrombolysis

Answer 59

Rupture of blood vessel within the brain leading to oxygen deprivation and infarction. Pooling of blood causes raised intracranial pressure. Raised ICP puts pressure on skull, brain and blood vessels causing tissue death. Raised ICP causes CSF herniation (hydrocephalus), midline shift, tentorial herniation (movement of tissue from one intracranial compartment to another), coning (brainstem compression)

Answer 60

Symptoms last over 24 hours. Sudden onset severe headache. Weakness of limbs, facial weakness, dysphagia (speech disturbance), visual or sensory loss. Raised ICP.

Answer 61

Symptoms: Severe headache, N+V, syncope, loss of consciousness, vertigo, meningism, coma

Answer 62

Non contrast head CT (distinguishes haemorrhagic from ischaemic stroke, shows site of haemorrhage) hyperdense blood on CT

Answer 63

1st line: Urgent non contrast head CT. Blood tests: FBC (look for polycythaemia, thrombocytopenia), glucose, ESR (raised in vasculitis), U&Es, cholesterol, lipid profile, INR (if on warfarin), prothrombin time. ECG (atrial fibrillation, myocardial infarction) Other: Glasgow coma scale (eyes, verbal, motor. Max 15/15. 8/15 requires securing the airway)

Answer 64

TIA, ischaemic stroke, complicated migraine, hypoglycaemia, hypertensive encephalopathy

Answer 65

1st line – confirm haemorrhagic on CT then neurosurgery referral Urgent lowering of blood pressure, IV mannitol to lower ICP, urgent anticoagulation reversal (clotting factor replacement)

Answer 66

Infection, deep vein thrombosis, pulmonary embolism, seizures

Answer 67

50% mortality

Answer 68

Epilepsy is an umbrella term for tendency to have seizures. Seizures are transient episodes of abnormal electrical activity in the brain. Types of focal seizure: simple partial, complex partial, partial seizure with secondary generalisation. Criteria, one of: At least 2 unprovoked seizures occurring more than 24hrs apart One unprovoked seizure and a probability of future seizures (considered >60% risk in 10yrs) Diagnosis of an epileptic syndrome

Answer 69

Onset at extremes of life <20yrs or >60yrs, partial focal seizures (60% of seizures)

Answer 70

2/3 idiopathic (often familial link), cortical scarring (trauma, cerebrovascular disease, infection), tumours, strokes, Alzheimer’s, alcohol withdrawal (delirium tremens)

Answer 71

Family history, premature babies, abnormal cerebral blood vessels, drugs e.g., cocaine

Answer 72

Normal balance between GABA (inhibitory) and glutamate (excitatory) shifts towards glutamate therefore increased glutamate stimulation and GABA inhibition causes increased excitation. Components of epileptic seizure: 1. Prodrome: precedes the seizure, usually hours/days, weird feeling e.g., mood, behaviour. 2. Aura: feeling before seizure starts. Strange feeling in gut, déjà vu, automatisms (lip smacking, rapid blinking), strange smells, flashing lights. Often implies partial seizure. 3. Post-ictal: period after seizure. Headache, confusion, myalgia, sore tongue (usually bitten), amnesia. Temporary weakness after focal seizure in motor cortex = Post-Ictal Todd’s palsy. Dysphasia following temporal lobe seizure.

Answer 73

Partial (focal): focal onset with features that can be referrable to a single lobe, e.g., temporal lobe. Often seen with underlying structural disease i.e., underlying cause Electrical discharge is limited to one lobe, in one hemisphere. These may later progress to become generalised seizures

Answer 74

Simple partial = no affect on consciousness or memory. Awareness unimpaired but will have focal motor, sensory, autonomic, or psychic symptoms depending on affected lobe. No post-ictal symptoms Complex partial = memory/awareness is impaired. Most commonly arises in temporal lobe > affects speech, memory, and emotion. Post-ictal confusion is common if temporal lobe, whereas recover is swift if frontal lobe is affected. Partial seizure with secondary generalisation = 2/3 patients with partial seizures will develop generalised seizures, usually tonic-clonic. These start focally and spread widely throughout the cortex. Specific lobe characteristics: Temporal – dysphasia, aura, automatisms, memory, emotion, speech Frontal – motor, jacksonian march (seizures march up and down motor homunculus), post-ictal Todd’s palsy (temporary focal weakness after seizure) Parietal –paraesthesia Occipital – visual phenomena e.g., spots, line, zigzags

Answer 75

Clinical diagnosis (at least 2 seizures more than 24hours apart) and EEG (focal spikes or sharp waves in affected area)

Answer 76

Electroencephalogram (supportive not diagnostic, can determine type of epileptic syndrome) MRI/CT (examine hippocampus, rule out other causes, e.g., tumour, bleeding) Bloods (rule out other causes - FBC, Ca2+, electrolytes, U&Es, LFTs, glucose) Genetic testing

Answer 77

Syncope, TIA, generalised seizures, sleep disorders, chorea

Answer 78

Usually only started after 2nd epileptic episode. 1st line – lamotrigine/carbamazepine. 2nd line – sodium valproate/levetiracetam

Answer 79

Status epilepticus: more than 3 seizures in one hour, or seizure lasting over 5 mins. (Tx: IV or rectal benzodiazepines e.g., lorazepam or diazepam. Alternative, phenytoin) Head trauma, fractures, memory loss

Answer 80

Epilepsy is an umbrella term for tendency to have seizures. Seizures are transient episodes of abnormal electrical activity in the brain. Types of general seizure: tonic, clonic, tonic-clonic, myoclonic, atonic, absence. Criteria, one of: At least 2 unprovoked seizures occurring more than 24hrs apart One unprovoked seizure and a probability of future seizures (considered >60% risk in 10yrs) Diagnosis of an epileptic syndrome

Answer 81

Onset at extremes of life, <20yrs or >60yrs. Primary general seizures (40% of seizures)

Answer 82

2/3 idiopathic (often familial link), cortical scarring (trauma, cerebrovascular disease, infection), tumours, strokes, Alzheimer’s, alcohol withdrawal (delirium tremens)

Answer 83

Family history, premature babies, abnormal cerebral blood vessels, drugs e.g., cocaine

Answer 84

Normal balance between GABA (inhibitory) and glutamate (excitatory) shifts towards glutamate therefore increased glutamate stimulation and GABA inhibition causes increased excitation. Components of epileptic seizure: 1. Prodrome: precedes the seizure, usually hours/days, weird feeling e.g., mood, behaviour. 2. Aura: feeling before seizure starts. Strange feeling in gut, déjà vu, automatisms (lip smacking, rapid blinking), strange smells, flashing lights. Often implies partial seizure. 3. Post-ictal: period after seizure. Headache, confusion, myalgia, sore tongue (usually bitten), amnesia. Temporary weakness after focal seizure in motor cortex = Post-Ictal Todd’s palsy. Dysphasia following temporal lobe seizure.

Answer 85

Primary generalised: simultaneous electrical discharge throughout the whole cortex, no features suggesting localisation to one hemisphere/lobe. Bilateral and symmetrical motor manifestations Always associated with loss of consciousness and lack of awareness

Answer 86

Tonic = high muscle tone, rigid, stiff limbs. Will fall to floor if standing due to stiff limbs. Clonic = rhythmic muscle jerking (i.e., clonus the UMN sign) Tonic-clonic (Grand Mal) = combination of tonic and clonic. Stereotypical shaking seizures due to mix of on/off rigidity and muscle jerking. Open eyes, incontinence, tongue bitten. Myoclonic = isolated jerking of a limb/face/trunk. ‘Disobedient limb’ or ‘thrown to floor’. Typically in juvenile myoclonic epilepsy. Atonic = opposite of tonic, loss of muscle tone = floppy Absence (Petit Mal) = common in childhood, increased risk of developing tonic-clonic seizures in adulthood. Will go pale and stare blankly for a few seconds. Often suddenly stop talking mid-sentence and do not realise they have had an attack. 3Hz spike on EEG.

Answer 87

Clinical diagnosis (at least 2 seizures more than 24hours apart) and EEG (determine type of seizure)

Answer 88

Electroencephalogram (supportive not diagnostic, can determine type of epileptic syndrome, e.g., 3Hz spike in absence seizure) MRI/CT (examine hippocampus, rule out other causes, e.g., tumour, bleeding) Bloods (rule out other causes - FBC, Ca2+, electrolytes, U&Es, LFTs, glucose) Genetic testing (e.g., for juvenile myoclonic epilepsy)

Answer 89

Focal seizures, non-epileptic seizures, convulsive syncope, cardiac arrhythmia, TIA

Answer 90

Usually only started after 2nd epileptic episode. 1st line – sodium valproate for all generalised seizures in males and women not childbearing age. Women of childbearing age: give lamotrigine for all generalised seizures except myoclonic (levetiracetam/topiramate) and absence (ethosuximide). Sodium valproate highly teratogenic

Answer 91

Status epilepticus: more than 3 seizures in one hour, or seizure lasting over 5 mins. (Tx: IV or rectal benzodiazepines e.g., lorazepam or diazepam. Alternative, phenytoin)

Answer 92

Progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movement.

Answer 93

Typically develops 55-65 years old

Answer 94

Loss of dopaminergic neurons from substantia nigra pars compacta in basal ganglia. Drug-induced Parkinson’s caused by dopamine antagonists e.g., clozapine. Also caused by encephalitis or exposure to certain toxins, e.g., manganese dust

Answer 95

Age, male sex, pesticide exposure

Answer 96

Basal ganglia are responsible for coordination of habitual movements e.g., walking, controlling voluntary movements and learning specific movement patterns. Substantia nigra pars compacta produces dopamine which is essential for the correct functioning of the basal ganglia. To initiate movement, SNPC signals to the striatum through the nigrostriatal pathway to stop firing to the substantia nigra pars reticulata and therefore stop inhibiting movement. If the SNPC is degenerated, there is decreased dopaminergic input which depressed the nigrostriatal pathway making it harder to initiate movement.

Answer 97

Symptoms are characteristically asymmetrical, one side affected more than other. Classic triad: resting tremor, rigidity, bradykinesia.

Answer 98

Signs: Impaired dexterity, fixed facial expressions, foot drag, postural instability. Shuffling gait with decreased arm swing on one side. Pill rolling thumb (rub thumb and finger back and forth). Cogwheel/lead pipe rigidity. Stooped posture. Forward tilt. Symptoms: Dementia, depression, urinary frequency, constipation, sleep disturbances, fatigue, impaired balance, lost sense of smell (hyposmia, anosmia)

Answer 99

Clinical diagnosis

Answer 100

1st line – dopaminergic agent trial 3 step diagnosis: 1. Diagnosis of parkinsonian syndrome: bradykinesia + one of rigidity, resting tremor, or postural instability 2. Exclusion criteria (none to be met): Hx stroke, repeated head injury, neuroleptic treatment, unilateral features after 3 years, cerebellar signs, Babinski’s sign, early severe dementia, negative response to large L-dopa dose. 3. Supportive criteria (3+ required): unilateral onset, rest tremor present, progressive, excellent response to L-dopa, visual hallucinations. Other: MRI brain, functional neuroimaging

Answer 101

Lewy body dementia (Parkinson Sx then dementia = Parkinson dementia. Parkinson sx after dementia = Lewy body dementia w/ Parkinson’s) Benign essential tremor, Wilson’s disease

Answer 102

1st line symptomatic management – levodopa (L-dopa) + peripheral decarboxylase inhibitor (prevents breakdown of levodopa so more is available at blood-brain barrier, e.g., carbidopa, benserazide). Body can become resistant to levodopa very quickly so give a COMT inhibitor alongside L-dopa to prevent weaning off. (e.g., entacapone) MAO-B inhibitor (rasagiline, selegiline) – prevents dopamine breakdown.

Answer 103

Too much dopamine – dyskinesias: dystonia (excess contractions), chorea (jerky), athetosis (twisting/writhing) as a result of levodopa treatment. Dementia. Bladder dysfunction. Dysphagia.

Answer 104

Most common type of dementia. Chronic neurodegenerative disease with an insidious onset and progressive but slow decline in cognitive function (memory, judgement, language).

Answer 105

Females, over 65

Answer 106

Beta-amyloid plaques, neurofibrillary tangles

Answer 107

Advanced age, Down’s syndrome, ApoE E4 allele homozygosity, reduced cognitive activity, depression/loneliness

Answer 108

Pathological landmarks: extracellular deposition of beta-amyloid plaques, tau-containing intracellular neurofibrillary tangles, damaged synapses, atrophy, cortical scarring, decreased Ach neurotransmitter. Accumulation of beta-amyloid plaques and neurofibrillary tangles leads to a reduction in information transmission and eventually the death of brain cells

Answer 109

Memory – episodic and semantic (language difficulties, general knowledge, fact recall). Language – difficulty understanding or finding words, dysphasia. Attention and concentrating issues. Psychiatric changes, e.g., withdrawal, delusions, personality change, apathy. Disorientation e.g., time and surroundings.

Answer 110

Signs: Agnosia (can’t recognise things), apraxia (can’t do basic motor skills), aphasia (speech problems)

Answer 111

Brain MRI (temporal lobe and cortical atrophy)

Answer 112

MMSE (mini mental state examination): score /30. >25 = normal. 18-25 = impaired. <18 = severely impaired. Tests communication, memory, activities of daily life. memory clinic assessment, Bloods – FBC, U&Es, B12 (rule out other causes), brain MRI

Answer 113

Delirium, depression, vascular dementia, Lewy body dementia, frontotemporal dementia

Answer 114

No cure. Supportive therapy – carers, changes to home, help with daily activities. Medication to manage symptoms – anticholinesterase inhibitors, e.g., donepezil, rivastigmine, galantamine, memantine

Answer 115

Pneumonia, institutionalisation, UTI, falls, weight loss, elder abuse

Answer 116

Primary headache. Recurrent throbbing headache often preceded by aura and associated with nausea, vomiting and visual changes.

Answer 117

Most common cause of episodic headache, more in females, onset before 40yo

Answer 118

CHOCOLATE: chocolate, hangovers, orgasms, cheese, oral contraceptives, lie-ins, alcohol, tumult e.g., loud noises, exercise

Answer 119

Genetics, FHx, Female, age (majority of first migraines are in adolescence), stress

Answer 120

Suggestion that migraines may be due to irritation of trigeminal nuclei within the brainstem due to changes in arterial blood flow, this is why there is the pattern of one side of face being affected. Arteries painfully dilate during migraine

Answer 121

At least 2 of: unilateral pain (usually 4-72hrs), throbbing-type pain, moderate > severe intensity, motion sensitivity Plus at least 1 of: nausea/vomiting, photophobia/phonophobia There must be a normal exam and no attributable cause.

Answer 122

Prodrome (days before): yawning, cravings, mood/sleep changes Aura (mins before attack – migraines classified as with or without aura): visual disturbances, e.g., lines, dots, zigzags. Somatosensory e.g., paraesthesia, pins and needles

Answer 123

Clinical diagnosis

Answer 124

1st line: Clinical diagnosis Other: Rule out other causes: labs e.g., ESR/CRP, CT/MRI indications: worst/severe/thunderclap headache, change in pattern of migraine, abnormal neurological exam, onset >50yrs, epilepsy, posteriorly located headache Lumbar puncture indications: thunderclap headache, severe rapid onset headache/progressive headache/unresponsiveness headache

Answer 125

Cluster headache, tension headache, subarachnoid haemorrhage, giant cell arteritis

Answer 126

1st line – triptans e.g., sumatriptan (MOA: 5HT (serotonin) receptor agonists - act on trigeminal nerve to prevent peptide release which would cause vasodilation and pain, and on cranial vasculature causing vasoconstriction) NSAIDs (naproxen), anti-emetic (metoclopramide), avoid opioids and ergotamine Prevention: required if >2 attacks per month OR require acute meds >2x per week: Beta blockers (propranolol), TCAs (amitriptyline), anti-convulsant (topiramate – CI pregnant)

Answer 127

Pregnancy complications (pre-eclampsia, low birth weight), depression, migraine-triggered seizures

Answer 128

At least one of: bilateral, pressing/tight and non-pulsatile (like an elastic band around head), mild/moderate intensity, +/- scalp tenderness. No aura, vomiting or head sensitivity to movement. Can be some ‘pressure’ behind eyes, but pain isn’t localised around eye

Answer 129

Stress, mental tension

Answer 130

Primary headache. Most common chronic and recurrent daily headache. Bilateral generalised pain, can spread to neck. Can be episodic <15 days/per month, or chronic >15 days/month (for at least 3 months)

Answer 131

Triggers: stress, sleep deprivation, bad posture, hunger, eyestrain, anxiety, noise, overexertion, tension in muscles of face/jaw/neck

Answer 132

Symptoms: Generalised head pain, frontal head pain, sinus region pain (star shape), neck muscle tenderness (trapezius, SCM)

Answer 133

Clinical diagnosis

Answer 134

If suspected pathology: CT sinus, MRI brain, lumbar puncture

Answer 135

Migraine, cluster headache, giant cell arteritis, sphenoid sinusitis

Answer 136

Avoid triggers and stress relief. Symptomatic relief: aspirin, paracetamol, ibuprofen, AVOID OPIOIDS Chronic: antidepressants (amitriptyline) Limit analgesics to no more than 6 days per month to reduce the risk of medication-overuse headaches

Answer 137

NSAIDs complications (peptic ulcer, GI bleed, kidney injury)

Answer 138

Primary headache. Clusters of episodic headaches lasting from 7 days up to 1 year (usually 2-3 weeks) with pain-free periods in between. Excruciating unilateral periorbital pain

Answer 139

Much rarer than migraines, more common in males, 20-40yrs, most debilitating headache

Answer 140

Smoker, alcohol, male, genetics (autosomal dominant gene link)

Answer 141

Hypothalamic activation with secondary trigeminal and autonomic activation.

Answer 142

Rapid onset of excruciating pain, classically around the eye (other common areas are temples and forehead) Pain is strictly unilateral and localised to one area (rises to a crescendo over a few minutes and lasts for 15mins-3hrs, 1-2 times a day, usually around the same time of day) Ipsilateral autonomic features: watery and bloodshot eye, facial flushing, rhinorrhoea (blocked nose), miosis (pupillary constriction), ptosis

Answer 143

Clinical diagnosis, at least 5 similar attacks (strictly unilateral, periorbital/supraorbital/temporal pain, lasting 15-180mins)

Answer 144

Rule out other causes: brain MRI, ESR, pituitary function tests

Answer 145

Migraine, tension headache, trigeminal neuralgia, subarachnoid haemorrhagic, giant cell arteritis

Answer 146

Acute attack – 15L 100% oxygen for 15mins via non-rebreather mask. Triptans e.g., sumatriptan Prevention – 1st line verapamil (CCB), lithium, topiramate, reduce alcohol and stop smoking

Answer 147

Depression

Answer 148

Type 4 hypersensitivity cell-mediated autoimmune condition characterised by repeated episodes of inflammation of the nervous tissue in the brain and spinal cord. Results in the demyelination of CNS.

Answer 149

Young females most common (20-40 years)

Answer 150

Unknown. Influenced by: genetic and environmental factors, EBV, smoking, obesity, low Vit D

Answer 151

Female 20-40yo, FHx, autoimmune conditions, EBV

Answer 152

Loss of myelin sheath in CNS. Oligodendrocytes (CNS) are affected, Schwann cells (PNS) are not affected. This slows or blocks the transmission of signals to and from the brain. 3 types of MS: 1. Relapsing-remitting MS: symptoms come and go, periods of good health followed by sudden symptoms, most common presentation. 2. Secondary progressive MS: flows from relaxing-remitting (50% develop secondary progressive), gradually worsening symptoms with fewer remissions 3. Primary progressive MS: from the beginning of the disease. Symptoms gradually develop and worsen over time. 10-15% of people at onset Acute attacks are followed by periods where remyelination occurs. With advancing disease, these periods get shorter and less frequent.

Answer 153

Optic neuritis 1st sx (optic nerve swelling – pain with eye movement, vision loss in one eye). Pyramidal weakness – upper limb extensors and lower limb flexors. Spastic paraparesis. Uhthoff phenomenon (symptoms worse with heat) MS lesions disseminated in time and space (different symptoms each attack, affecting different parts of CNS)

Answer 154

Signs: UMN signs. Loss of colour vision. Lhermitte sign (electric jolt felt down the spine when flexing neck). Eye movement abnormalities due to 6th cranial nerve palsy (abducens) - Internuclear ophthalmoplegia, conjugate lateral gaze disorder. Charcot neurological triad: nystagmus, intention tremor, dysarthria Symptoms: Changes in sensation/numbness/tingling. Paraesthesia. Fatigue. Chronically increasing bladder involvement. Cognitive impairment. Dizziness. Depression.

Answer 155

McDonald criteria: symptoms disseminated in time (>1 month apart) and space (damage to different parts of CNS seen on MRI). GS tool = MRI brain and spinal cord

Answer 156

Bloods should be normal: FBC, U&Es, LFTs, TFTs, B12, HIV serology, calcium, glucose. Lumbar puncture (oligoclonal IgG bands in CSF), MRI, evoked potentials (measures brain electrical activity in response to stimulation of sight, sound or touch).

Answer 157

Fibromyalgia, Sjogren syndrome, Vitamin B12 deficiency, peripheral neuropathy, ischaemia stroke

Answer 158

General management: MDT care, supportive therapy, legal obligation to inform DVLA. Acute relapses – steroids (IV methylprednisolone). Relapsing-remitting MS: interferon beta (CI in pregnancy), DMARDs, biologics (IV natalizumab), oral fingolimod (immunomodulator) Secondary progressive MS: Siponimod or methylprednisolone. Primary progressive MS: ocrelizumab

Answer 159

UTI, osteoporosis, depression, visual impairment, erectile dysfunction, cognitive impairment, reduced motility

Answer 160

A group of neurodegenerative diseases affecting upper and lower motor neurons. Most cases are Amyotrophic Lateral Sclerosis (ALS). Other cases are: Progressive Bulbar Palsy (PBP), Primary Lateral Sclerosis (PLS), Progressive Muscular Atrophy (PMA).

Answer 161

Men slightly more affected (3:2). Common onset 40-50 (familial) or 58-63 (sporadic)

Answer 162

Sporadic. Few familial variants: SOD-1 gene, C90RF72 gene

Answer 163

Mostly affects anterior horn cells of the spinal cord and the motor cranial nuclei. Progressive bulbar palsy affects the medulla oblongata – origin of cranial nerves 9-12. Worse prognosis. Motor neuron disease never affects: 1. Eye muscles (multiple sclerosis and myasthenia gravis do). 2. Sensory functions (multiple sclerosis and polyneuropathies do)

Answer 164

Mixed upper and lower motor neuron presentations, LMN predominates, e.g., weakness, muscle atrophy, fasciculations. Onset in the limb is the typical presentation, e.g., wrist/foot drop, change in appearance of hands – wasting, gait disorders/tripping, excessive fatigue.

Answer 165

Signs: Amyotrophic Lateral Sclerosis (ALS): UMN and LMN, asymmetrical, Babinski +ve (stroke foot – toe extension), tongue fasciculations, corticobulbar signs: brisk jaw reflex, dysarthria, dysphagia, sialorrhea (excessive saliva), progressive paralysis, eventually respiratory failure. Progressive Bulbar Palsy (PBP): LMN in brain stem, pharyngeal muscle weakness, progressive loss of speech, tongue atrophy, trouble with talking, chewing, swallowing. Primary Lateral Sclerosis (PLS): UMN of arms/legs/face, slower movements, pseudobulbar effects (uncontrolled laughing or crying), UMN signs Progressive Muscular Atrophy (PMA): LMN only, muscle wasting, clumsy hand movements, fasciculations, muscle cramps

Answer 166

El Escorial criteria: 1. Presence of: LMN degeneration by clinical, electrophysiological, or neuropathological examination; UMN degeneration by clinical examination; progressive symptoms as determined by the history. 2. Absence of: electrophysiological and pathological evidence of other diseases processes; neuroimaging evidence of disease processes

Answer 167

Nerve conduction studies, electromyogram (shows fibrillation potentials), CT/MRI brain and spinal cord (other causes), bloods (other causes), muscle biopsy

Answer 168

Myasthenia gravis, multifocal motor neuropathy, inclusion body myositis

Answer 169

MDT care, supportive therapy, occupational, speech and language, physiotherapy, nutrition support (PEG tube - through stomach). Non-invasive ventilation. Riluzole (neuroprotective glutamate-release inhibitor, life-prolonging treatment). Quinine/baclofen (cramps). Hyoscine (sialorrhea – drooling)

Answer 170

Respiratory failure, aspiration pneumonia, swallowing failure, nutritional deficit

Answer 171

2-4 years post-diagnosis

Answer 172

Inflammation of the meninges lining the brain and spinal cord, due to bacteria, viral or fungal infection. Notifiable disease.

Answer 173

Infants and teenagers most at risk. Viral is most common, bacterial is more serious

Answer 174

Bacterial meningitis: N. meningitidis, E. Coli, listeria, haemophilus influenza B, s. pneumonia, klebsiella, TB Viral meningitis: mumps, herpes zoster, influenza, HIV, measles, enteroviruses (coxsackie) Fungal meningitis: cryptococcus, candida, histoplasma

Answer 175

Immunosuppression, smoking, CSF shunts, diabetes mellitus, IVDU, adrenal insufficiency, malignancy, sickle cell disease, crowding (university!)

Answer 176

Neisseria meningitis is a gram-negative diplococcus bacteria. Meningococcal septicaemia is when meningococcus is in the bloodstream and causes a non-blanching rash which indicates the infection has disseminated intravascular coagulation and subcutaneous haemorrhages.

Answer 177

Stiff neck, photophobia, headache, pyrexia, Kernig sign (pain on passive leg extension when knee is flexed), Brudzinski sign (passive flexion of neck causes hip and knee flexion)

Answer 178

Signs: non-blanching purpuric rash (meningococcus only), septic shock. Raised ICP: decreased GCS, seizure, focal deficits, cranial nerve palsies Symptoms: Fever, headache, nausea, vomiting, lethargy, irritability, muscle pains, chills, shivering, sore throat, decreased consciousness

Answer 179

Lumbar puncture (L3/L4) and CSF analysis. Contraindicated with raised ICP, shock

Answer 180

If suspected do not delay treatment – IV antibiotics before lumbar puncture. Lumbar puncture within 1 hour of arrival. Blood cultures (positive). FBC (leucocytosis, anaemia, thrombocytopenia), U&E (acidosis, hypokalaemia, hypocalcaemia, hypomagnesemia), Glucose, lactate dehydrogenase, LFTs. ABG (acidosis), clotting screen (DIC). Pneumococcal and meningococcal PCR. Viral PCR. Fungal cultures (3 sets)

Answer 181

Encephalitis, bacterial/viral/fungal/tuberculosis meningitis

Answer 182

1st line – empirical antibiotics. With rash = Benzylpenicillin IV. Without rash = Cefotaxime IV. Plus, steroids (dexamethasone) for bacterial meningitis. Add vancomycin is S. pneumoniae suspected. Add amoxicillin if listeria suspected. Prophylactic antibiotics for household/contacts. No specific treatment for viral meningitis. Analgesia, antipyretics, hydration

Answer 183

Disseminated intravascular coagulation, meningococcal septicaemia, Waterhouse Friedrichsen syndrome (adrenal insufficiency caused by adrenal haemorrhage from meningococcal DIC). Hearing loss, seizures, cognitive impairment and learning disability, memory loss.

Answer 184

20-30% mortality

Answer 185

Inflammation of brain parenchyma

Answer 186

Most severe infections in children and elderly. Most commonly HSV-1

Answer 187

Viral infection (most commonly HSV-1 herpes simplex virus. Also, CMV, EBV). TB, Lyme disease, toxoplasmosis, ticks

Answer 188

Immunocompromised, extremes of age

Answer 189

Virus gains entry via skin/GI/GU/resp tract and spreads to brain via haematogenous spread

Answer 190

Triad of fever, headache, altered mental status. Rash

Answer 191

Signs: Raised ICP. Encephalopathy. Focal neurology (temporal lobe – aphasia) Symptoms: Meningitis symptoms (neck stiffness, photophobia, vomiting, headache). Reduced consciousness, drowsiness, coma. Cough

Answer 192

MRI brain (swelling of brain)

Answer 193

1st line: Bloods – FBC (raised WCC), U&Es (hyponatraemia), LFTs, TFTs, B12, lactate Lumbar puncture and CSF analysis – viral PCR to detect virus (lymphocytosis with normal CSF:plasma glucose ratio) Blood cultures. EEG (background slowing). HIV testing

Answer 194

Meningitis, encephalopathy, ischaemic stroke

Answer 195

1st line – aciclovir as soon as encephalitis suspected. Confirmed HSV-1 = aciclovir. Varicella zoster = aciclovir/ganciclovir. CMV = ganciclovir. EBV = aciclovir/ganciclovir Non-viral encephalitis = antibiotics – IV benzylpenicillin.

Answer 196

Seizures, neurological problems (aphasia, memory loss, motor problems), hydrocephalus

Answer 197

Primary brain tumours: gliomas – astrocytoma (most common), oligodendroglioma. Others – ependymoma, meningioma, schwannoma, craniopharyngiomas Secondary brain tumours: non-small cell lung cancers (most common), small cell lung cancer, breast, melanoma, renal cell carcinoma, GI

Answer 198

Secondary brain tumours much more common

Answer 199

Gliomas are tumours of glial cells of brain and spinal cord: astrocytoma (glioblastoma multiforme most common), oligodendroglioma, ependymoma.

Answer 200

Raised ICP, Cushing triad (bradycardia, raised pulse pressure, irregular breathing), focal neurology, epileptic seizures, lethargy, weight loss, papilloedema (swelling of optic disc), CN6 palsy.

Answer 201

MRI head to locate tumour then biopsy to determine grade

Answer 202

No lumbar puncture due to raised ICP = massive contraindication

Answer 203

1st line – surgery to remove tumour and decrease ICP. + chemo before/after/during surgery Dexamethasone + mannitol to decrease ICP

Answer 204

Transient unilateral vision loss caused by temporary occlusion of the retinal artery. Like a curtain coming down.

Answer 205

Blood clot or plaque in retinal artery, heart disease, stroke, hypertension, high cholesterol

Answer 206

Often signal a stroke is impending as it is caused by a clot blocking the artery to the eye

Answer 207

1st line – aspirin to prevent blood clots

Answer 208

Compression of the spinal cord from C1-L1/2

Answer 209

Vertebral body tumours (most common spine malignancies are breast, prostate, and lung cancer) Trauma, central disc protrusion, prolapsed disc (L4-5 and L5-S1 most common), epidural haematoma, infection, cervical spondylitic myelopathy

Answer 210

Pressure on spinal cord causes the nerves to swell which slows down or blocks their blood supply, causing the nerves to stop working properly.

Answer 211

Red flag: progressive limb weakness, UMN signs in lower limbs (e.g. clonus, hyperreflexia, Babinski sign) LMN signs in upper limbs (e.g. atrophy). Sensory loss below lesion (as ascending tracts send info up). Loss of bladder/bowel function

Answer 212

Paraplegia, back pain, paraesthesia, changes to tendon reflexes

Answer 213

MRI spine (visualise cord compression)

Answer 214

X-ray whole spine, MRI spine, RFTs, haemoglobin – monitor blood loss

Answer 215

Guillain-Barre syndrome, transverse myelitis, intervertebral disc herniation/compression

Answer 216

1st line – dexamethasone until treatment plan confirmed. Catheterisation, analgesia, surgical decompression (laminectomy, microdiscectomy), chemotherapy if indicated

Answer 217

Pressure ulcers, autonomic dysfunction, DVT, falls

Answer 218

Surgical emergency where the nerves roots of the cauda equina at the end of the spinal cord are compressed. L2/3 downwards

Answer 219

Lumbar herniation at L4/5 or L5/S1, tumours, trauma, infection/abscess, spondylolisthesis

Answer 220

The cauda equina is formed by the nerve roots below spinal cord termination conus medularis at L2/3. Nerve roots exit either side of spinal column at their vertebral level (L4, L5, S-5 and Co). The nerves of cauda equina supply: sensation to lower limbs, perineum, bladder and rectum. Motor innervation to the lower limbs and the anal and urethral sphincters. Parasympathetic innervation of bladder and rectum.

Answer 221

Sudden onset. Saddle paraesthesia (loss of perineum sensation). Bilateral LMN weakness, absent ankle reflex (L5-S1), hypotonia, fasciculations. Bladder/bowel dysfunction + sphincter involvement (loss of sensation, incontinence, reduced anal tone).

Answer 222

Lower back pain, sexual dysfunction, leg weakness, bilateral sciatica

Answer 223

MRI spine (visualisation of lesion and nerve compression)

Answer 224

Medical emergency – immediate referral. Urgent MRI spine. Rectal exam – loss of anal tone/sensation. Testing nerve roots and reflexes (absent ankle reflex L5-S1).

Answer 225

Spinal compression fracture, Guillain-Barre, transverse myelitis

Answer 226

1st line – surgical decompression (microdiscectomy/spinal fixation). Immobilize spine. VTE prophylaxis, antibiotics if infection

Answer 227

Bladder/bowel/sexual dysfunction, back or leg pain, sensory loss, leg weakness

Answer 228

Damage to a nerve through compression, trauma, infection etc. resulting in interruption of axonal continuity

Answer 229

Nerves 3-12 in brainstem therefore brainstem pathology e.g. trauma, tumour, multiple sclerosis

Answer 230

1. Olfactory: impaired/lost sense of smell 2. Optic: blindness, visual field defects 3. Oculomotor: ptosis, down + out eye, fixed dilated pupil 4. Trochlear: diplopia looking down, always due to trauma 5. Trigeminal: jaw deviates to affected side, loss of corneal reflex, causes: trigeminal neuralgia: sensory pain/motor jaw pain in V1/2/3 6. Abducens: adducted eye, inability to look laterally, sign of raised ICP 7. Facial: facial droop with forehead sparing, causes: bell’s palsy, parotid inflammation 8. Vestibulocochlear: hearing loss, loss of balance, causes: skull changes, (e.g., Paget’s), compression, middle ear disease 9. Glossopharyngeal: impaired gag reflex 10. Vagus: impaired gag reflex, swallowing, respiration, vocal issues, causes: jugular foramen lesion 11. Accessory: can’t shrug shoulders or turn head against resistance 12. Hypoglossal: tongue deviation towards affected side

Answer 231

Neurological examination, MRI

Answer 232

Medication (anti-convulsants, analgesia), surgery, physiotherapy.

Answer 233

Compression of the median nerve (C5-T1) in the carpal tunnel

Answer 234

Females 40-60s, pregnant women

Answer 235

Swelling of carpal tunnel contents, narrowing of carpal tunnel

Answer 236

Female, hypothyroidism, acromegaly, obesity, pregnancy, rheumatoid arthritis, repetitive strain

Answer 237

8 carpal bones in wrist and transverse carpal ligament/flexor retinaculum that runs across the front. Between the carpal bones and ligament is the carpal tunnel. Capral tunnel contains median nerve and flexor tendons of forearm. Median nerve gives sensation to thumb, index finger, middle finger, and half of ring finger. Motor innervation to thenar muscles.

Answer 238

Paraesthesia, index and middle finger tend to be affected first. Pain in index and middle finger, can spread to shoulder. Numbness. Weakness of thenar muscles, loss of grip.

Answer 239

Signs: Wasting of thenar eminence Symptoms: Aching hand/forearm. Worse at night, relieved by hanging over side of bed. Wake and shake.

Answer 240

Electromyogram (slowing of conduction velocity across median nerve in carpal tunnel)

Answer 241

Clinical diagnosis based on symptoms: Phalen test: flex fist at wrist for 1 min. Positive = pain and paraesthesia. Tinel test: tapping wrist causes tingling. Nerve conduction test, electromyogram, USS or MRI if other damage suspected.

Answer 242

Osteoarthritis, ulnar neuropathy, polyneuropathy

Answer 243

1st line –Wrist splint at night. Steroid injections. Rest wrist, avoid gripping/squeezing movements. Surgery in severe cases to decompress carpal tunnel. ¼ cases are self-limiting. Pregnancy cases will resolve post-partum.

Answer 244

Difficulty lifting the front part of the foot, resulting in dragging of toes. Caused by damage to common peroneal nerve L4-S2 (common fibular nerve)

Answer 245

Injury, lower back damage, tumour, hip replacement, cauda equina syndrome, multiple sclerosis

Answer 246

Unilateral symptoms. One foot dragging across floor when walking. Tripping. Ipsilateral numbness and weakness.

Answer 247

Foot drop on clinical examination

Answer 248

Clinical diagnosis (foot drop). Underlying cause: X-ray, USS, MRI. Nerve conduction studies.

Answer 249

1st line – brace or splint. Physiotherapy. Specialised shoes (prevent foot drop when walking). Nerve stimulation. Surgery if indicated.

Answer 250

Autoimmune condition causing disorders of neuromuscular transmission due to the binding of autoantibodies to components of the neuromuscular junction, most commonly the acetylcholine receptor.

Answer 251

Peak incidence 40s for women and 60-70 for men

Answer 252

Females (autoimmune), males (thymoma)

Answer 253

Family history, other autoimmune conditions, thymoma

Answer 254

85% anti-acetylcholine receptor: bind to post synaptic receptor and competitively inhibit ACh binding. More receptors are blocked during exertion leading to more muscle weakness. These antibodies activate the complement system which damages cells at postsynaptic membrane. 15% anti-MuSK (muscle-specific kinase): MuSK helps synthesis acetylcholine therefore there will be decreased acetylcholine receptor expression on post-synaptic membrane.

Answer 255

Muscle weakness that gets worse with exercise and better with rest. Starts at head and neck, progresses to lower body. Ocular manifestations (weak eye muscles > diplopia, ptosis). Weakness is more marked in proximal muscles: small muscles of hands, deltoid and triceps, bulbar muscles (head and neck), muscles involved in chewing.

Answer 256

No muscle wasting, sensation unimpaired, myasthenia snarl (difficulty smiling, looking creepy), jaw fatigability, swallowing difficulty, speech fatiguability, seizures

Answer 257

Serology: acetylcholine receptors antibodies or muscle-specific kinase antibodies

Answer 258

Clinical diagnosis. Serology: detection of ACh receptor or MuSK antibodies. Crushed ice test: ice is applied to ptosis for 3 mins, if it improves it is likely myasthenia gravis. Tensilon/Edrophonium test: administer edrophonium – rapid acting acetylcholinesterase inhibitor. Positive = increased muscle power in a few secs for a few secs. CT thymus. Pulmonary function tests.

Answer 259

Lambert-Eaton myasthenic syndrome (autoimmune vs Ca2+ channels, sx improve with exertion. Associated with SCLC not thymoma. Sx start at extremities. Tx = steroids)

Answer 260

1st line –acetylcholinesterase inhibitors, e.g., Pyridostigmine or neostigmine (increases ACh and decreases muscle weakness). Immunosuppression (prednisolone or azathioprine). Rituximab. Thymectomy.

Answer 261

Myasthenic crisis: acute symptoms worsening with severe respiratory weakness. Tx = plasma exchange and IV immunoglobulins. BiPAP ventilation (bilevel positive airway pressure)

Answer 262

Damage to peripheral nerves resulting in transmission blockages between CNS and PNS

Answer 263

Diabetic neuropathy most common. Dietary deficiencies (B12 deficiency – axonal degeneration), medicines, alcohol excess, trauma, infection (e.g., shingles), Guillain Barre and Charcot-Marie-Tooth cause demyelination.

Answer 264

Mechanisms of peripheral neuropathy: demyelination, axonal damage, nerve compression, vasa nervosum infarction, Wallerian degeneration

Answer 265

Sensory: loss of touch, proprioception, temperature/pain sensation, paraesthesia. Numbness, tingling, burning/shooting pains. +ve Romberg test (patient cannot stand with feet together and eyes closed) – sensory ataxia. Motor: distal weakness – tripping, difficulty opening jars. Proximal weakness – difficulty climbing stairs. Muscle wasting. Fasciculations. Absent tendon reflexes.

Answer 266

Nerve conduction studies

Answer 267

Bloods – FBC, glucose, U&Es, LFTs, TFTs, B12, ESR. Nerve conduction studies. Electromyography (measures muscle electrical activity). Nerve biopsy.

Answer 268

Mononeuritis multiplex – damage to at least 2 different areas of peripheral nervous system. Causes (WARDS PLC): Wegener’s vasculitis, AIDS/amyloidosis, rheumatoid arthritis, DMT2, sarcoidosis, polyarteritis nodosa, leprosy, carcinomas. Symptoms = numbness, weakness, pain Dx= clinical presentation + nerve biopsy

Answer 269

1st line – treat underlying cause. Anti-seizure meds (Pregabalin/gabapentin). Antidepressants (amitriptyline). Supportive therapy, e.g., walking aids

Answer 270

Event of temporarily losing consciousness due to a disruption of blood flow to the brain, often leading to a fall

Answer 271

Primary syncope (simple fainting): dehydration, missed meals, extending standing in a war environment, vasovagal response to stimuli, e.g., sudden surprise, pain, sight of blood. Secondary syncope: hypoglycaemia, anaemia, infection, anaphylaxis, arrhythmias, valvular heart disease, hypertrophic cardiomyopathy

Answer 272

When the vagus nerve receives a strong stimulus it stimulates the parasympathetic nervous system which causes vasodilation of blood vessels in the brain. The blood pressure in cerebral circulation drops, leading to hypoperfusion of the brain tissue leading to loss of consciousness and fainting.

Answer 273

Prodrome: hot or clammy, sweating, heavy, dizzy, lightheaded, vision going blurry or dark, headache. Loss of consciousness and falling to the ground

Answer 274

History and clinical examination, ECG (arrhythmia, long QT syndrome), echocardiogram, bloods: FBC (anaemia), electrolytes (arrhythmias, seizures), blood glucose

Answer 275

Seizures, bradycardia, supraventricular tachycardias, ventricular tachycardias

Answer 276

Education and avoid triggers: dehydration, missing meals, standing still for long periods

Answer 277

Autosomal dominant condition causing progressive degeneration of the nervous system. 100% penetrance (all genotypes will express phenotype)

Answer 278

Onset 30-50yo

Answer 279

Autosomal dominant mutation. Trinucleotide expansion repeats: CAG repeats on Huntington’s gene on chromosome 4. More than 35 CAG repeats = Huntington’s. Anticipation: successive generations have more CAG repeats in the HTT gene, resulting in earlier onset and greater severity of disease.

Answer 280

Family history

Answer 281

Associated with cell loss within cortex and basal ganglia. Essentially too much dopamine. Lack of GABA and excessive nigrostriatal pathway.

Answer 282

Hyperkinesia. Chorea, dystonia, and incoordination. Depression, psychiatric issues.

Answer 283

Signs: Cognitive impairment, behavioural difficulties, psychosis. Eye movement disorders, dysarthria, dysphagia. Symptoms: Depression, irritability, agitation, anxiety.

Answer 284

Clinical diagnosis and genetic testing

Answer 285

Clinical diagnosis. MRI/CT brain – loss of striatal volume. Genetic testing (>35 CAG repeats on chromosome 4)

Answer 286

SLE, Wilson's disease, Sydenham's chorea

Answer 287

No treatment for stopping or slowing progression of disease. Chorea: antipsychotics (olanzapine), benzodiazepines (diazepam), dopamine antagonists (tetrabenazine) Psychosis: antipsychotics (haloperidol). Depression: SSRIs (citalopram)

Answer 288

Pneumonia, heart failure, MI, suicide

Answer 289

Poor prognosis: 15–20-year life expectancy after onset. Most common from respiratory failure, e.g., pneumonia. 2nd most common from suicide.

Answer 290

Acute polyneuropathy causing rapid damage of the peripheral nerves. Results in demyelination and axonal degeneration.

Answer 291

Males, peak ages 15-35 and 50-75

Answer 292

Commonly presents post-GI infection (approx. 6 weeks after). Most commonly campylobacter jejuni. Also caused by EBV, CMV, mycoplasma and HIV.

Answer 293

GI infection

Answer 294

Molecular mimicry: The B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection. These antibodies also match proteins on the nerve cells. They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon. Movement, sensation, and organ function can all be affected based on the nerves damaged.

Answer 295

Weakness, paraesthesia, hyporeflexia. Sudden onset toes to nose ascending symmetrical weakness. Loss of deep tendon reflexes. Peripheral loss of sensation or neuropathic pain. Cranial nerve facial weakness.

Answer 296

Signs: Absent reflexes (LMN sign). Involvement of autonomic nervous system: reduced sweating, reduced heat tolerance, paralytic ileus (pseudo-obstruction), urinary hesitancy. Respiratory failure Symptoms: Pain in legs, back pain rare, altered consciousness, ataxia (motor coordination difficulties), fatigue

Answer 297

Brighton criteria: clinical symptoms + Lumbar puncture CSF analysis + nerve conduction studies

Answer 298

Bloods – FBC, U&Es, LFT (raised AST and ALT). Stool culture. Lumbar puncture – cyto-protein dissociation: raised protein >0.55g/L. Normal WCC at <5 WBC per mm2. Nerve conduction studies (reduced conduction velocities, downwards conduction block). Spirometry for respiratory function. ECG

Answer 299

Myasthenia gravis, Lambert-Eaton myasthenic syndrome, transverse myelitis

Answer 300

1st line – IV immunoglobulin 0.44g/kg/day for 5 days and plasmapheresis DVT prophylaxis – LMWH. Avoid corticosteroids.

Answer 301

Respiratory failure, bladder areflexia (can’t contract), adynamic ileus, DVT, paralysis

Answer 302

85% recover

Answer 303

Hemisection of the spinal cord. Mostly in cervical region

Answer 304

Penetrating trauma

Answer 305

1. Ipsilateral hemiplegia (corticospinal tract). 2. Contralateral pain and temperature sensation deficits (spinothalamic tract). 3. Ipsilateral loss of proprioception, fine touch and vibration (dorsal column medial lemniscus tract)

Answer 306

Total ipsilateral loss of two-point discrimination, fine touch and vibration sensation at level of lesion. (DCML) Contralateral loss of pain and temperature below the lesion (spinothalamic) Sphincter disturbances, ipsilateral spastic paraparesis (muscle weakness with spasms), ipsilateral motor weakness (UMN)

Answer 307

MRI spine and neurological exam

Answer 308

Bloods: FBC, U&Es, LFTs, CRP/ESR, B12. Plain radiographs for penetrating or blunt trauma. MRI to examine extent of injury. Neurological examination to examine level of injury.

Answer 309

Stroke, multiple sclerosis, transverse myelitis, hemiplegia

Answer 310

1st line - Surgery (Spine immobilisation, decompression). Steroids to decrease swelling (IV methylprednisolone). Physical/occupational therapy.

Answer 311

Inherited disease affecting the peripheral sensory and motor nerves due to dysfunction in the myelin or the axons. PNS neuropathy

Answer 312

Childhood-adult onset

Answer 313

Autosomal dominant mutation

Answer 314

High foot arch (pes cavus), distal muscle wasting causing ‘inverted champagne bottle legs’, lower leg weakness, loss of ankle dorsiflexion (foot drop), weakness in hands, reduced tendon reflexes, reduced muscle tone, peripheral sensory loss. Walking difficulties, steppage gait (inability to lift foot while walking due to loss of dorsiflexion)

Answer 315

Nerve conduction studies, genetic testing

Answer 316

No treatment. Physiotherapy, occupational therapy, podiatry, orthopaedic surgery

Answer 317

Ulnar nerve palsy (C8-T1) presenting as claw hand

Answer 318

Ulnar nerve provides motor innervation to part of forearm and majority of hand. Sensory innervation to medial forearm, medial wrist, and medial 1.5 digits

Answer 319

Claw hand (4th and 5th fingers claw up), difficulty straightening fingers. Paraesthesia, tingling, numbness along forearm, into wrist, ring and little finger.

Answer 320

Clinical examination + electromyography/nerve conduction studies

Answer 321

1st line - splint and simple analgesia

Answer 322

Depressive disorders are characterised by persistent low mood, loss of interest and enjoyment, and reduced energy causing social and occupational dysfunction

Answer 323

20% of women, 12% of men

Answer 324

Combination of genetics, biological, environmental, psychological

Answer 325

Postnatal status, family history, dementia, stress

Answer 326

Main neurotransmitters (monoamines): serotonin (obsessions and compulsions), norepinephrine (anxiety and attention), dopamine (attention, motivation, and pleasure)

Answer 327

Depressed mood, lack of interest/pleasure (anhedonia), weight loss/gain, inability to sleep/oversleeping, psychomotor agitation/impairment, fatigue, feelings of worthlessness or guilt, decreased concentration, thoughts of death or suicide. Symptoms impact patient’s daily life

Answer 328

Criteria from diagnostic and statistical manual for mental disorders 5th edition: a. 5 of 9 symptoms most of the day, nearly every day: 1. depressed mood, 2. diminished interest/pleasure, 3. weight loss/gain, 4. inability to sleep/oversleeping, 5. psychomotor agitation/impairment, 6. fatigue, 7. feelings of worthlessness/guilt, 8. decreased concentration, 9. thoughts of death or suicidality (thoughts or attempts) b. symptoms cause significant distress to daily life c. not due to substance or other medical conditions d. symptoms cannot be better explained by other mental disorder e. no manic or hypomanic episodes

Answer 329

1. non-pharmacological: physical activity, healthy eating habits, psychotherapy/talk-therapy (CBT, interpersonal therapy) 2. pharmacological therapy: antidepressants. Selective serotonin reuptake inhibitors (SSRIs inhibit reuptake of serotonin so there is more in the synaptic cleft). E.g., citalopram, escitalopram, fluoxetine Monoamine oxidase inhibitors (MAO-Is). E.g, isocarboxazid, phenelzine Tricyclic antidepressants. E.g., amitriptyline 3. electroconvulsive therapy (electrical induced seizures)

Answer 330

X-linked recessive condition characterised by progressive muscle wasting and weakness

Answer 331

Young males, presents around 3yo

Answer 332

X-linked recessive

Answer 333

Results in damage to dystrophin gene so no dystrophin is produced. Dystrophin function - strength muscle fibres and protect from injury. Muscle replaced with adipose.

Answer 334

Presents early childhood. Progressive proximal muscular dystrophy with characteristic pseudohypertrophy of the calves. Major milestones delayed. Imbalance of lower limb strength. Recurrent falls. Speech delay. Fatigue. Gower’s sign: difficulty getting up from lying down (downward dog, use hands on knees to get up). Toe walking, hypotonia.

Answer 335

Genetic analysis

Answer 336

Serum creatinine kinase (very high). Muscle strength test. Gait assessment. Muscle biopsy with assay for dystrophin protein

Answer 337

Vitamin D and bisphosphonates for bone health. Corticosteroids. Immunisations – influenza and meningococcal. MDT care, specialist referral, physiotherapy, wheelchair, nutritional, palliative care

Answer 338

Joint contractures, respiratory failure, cardiomyopathy, heart failure, gastric dilation, learning difficulties, steroids: constipation, osteoporosis, hypertension.

Answer 339

Wheelchair by 12, death by 30

Answer 340

Neurodegenerative brain disorder. Progressive dementia common in under 65s. Causes atrophy of frontal and temporal lobes.

Answer 341

Common dementia in under 65s

Answer 342

Neuron damage and death in frontal and temporal lobe, genetic

Answer 343

Family history, autosomal dominant inheritance (Tau protein - chromosome 17) FHx of motor neuron disease

Answer 344

Pathological features: atrophy of frontal and temporal lobes, loss of neurons but no plaque formation.

Answer 345

Insidious and progressive onset. Behavioural issues: loss of inhibition/empathy, compulsive behaviours, difficulty planning Progressive aphasia: slow, difficult speech, grammatical errors Semantic dementia: loss of vocabulary, problems understanding words, problems recognising objects/faces Parkinsonism, memory impairment, disorientation

Answer 346

Brain MRI (temporal and frontal atrophy)

Answer 347

MMSE (mini mental state examination): score /30. >25 = normal. 18-25 = impaired. <18 = severely impaired. Tests communication, memory, activities of daily life. Bloods – FBC, U&Es, B12, LFTs (rule out other causes), brain MRI

Answer 348

Alzheimer’s, Lewy body dementia, vascular dementia, bipolar, OCD

Answer 349

No cure. Supportive therapy: carers, occupational therapy, speech and language therapy, stop exacerbating drugs. SSRIs (selective serotonin reuptake inhibitors) e.g., citalopram, sertraline – behavioural symptoms Levodopa/carbidopa – Parkinson’s symptoms

Answer 350

Financial crisis, dangerous driving, parenting problems

Answer 351

Rare disorder of neuromuscular transmission caused by impaired presynaptic release of acetylcholine

Answer 352

Autoimmune attack on presynaptic voltage gated calcium channels

Answer 353

Commonly presents with small cell lung cancer. Antibodies against voltage gated calcium channels in small cell lung cancer cells attack voltage gated calcium channels in the presynaptic terminal of the NMJ where motor and nerve cells communicate. When the VGCC are destroyed, less acetylcholine is released into the synapse causing less muscle contractions.

Answer 354

Insidious onset (comes on slowly), proximal muscle weakness, depressed tendon reflexes, gait changes, dry mouth, impotence in males, eyelid drooping (ptosis), dysphagia. Symptoms improve with exertion. Symptoms start at extremities then move to head and neck.

Answer 355

Serum test for VGCC antibodies (positive). Nerve conduction studies. Nerve stimulation. CT for malignancy Detection of ACh antibodies indicates myasthenia gravis but some LEMS patients have it too.

Answer 356

Myasthenia gravis

Answer 357

Amifampridine (allows more Ach to be released into NMJ). Plasma exchange, IV immunoglobulin, immunosuppression (prednisolone/azathioprine)

Answer 358

Neurodegenerative disorder with parkinsonism, progressive cognitive decline, executive dysfunction, behavioural and sleep problems, and visuospatial impairment. Characterised by presence of Lewy bodies

Answer 359

Lewby bodies deposited in brain

Answer 360

Old age, family history

Answer 361

Pathological features: Characterised by eosinophilic intracytoplasmic neuronal inclusion bodies (Lewy bodies) in the brainstem and cortex. Substantia nigra depigmentation and amyloid deposits. Lewy body dementia is on a spectrum: dementia first then parkinsonism is Lewy body dementia with parkinsonism, parkinsonism as the presenting complaint is Parkinson dementia.

Answer 362

Dementia often presents initially: memory loss, spatial awareness difficulties, loss of cognitive function, behavioural problems, visual hallucinations, sleep disorders Parkinsonism: bradykinesia, rigidity, resting tremor, change in gait

Answer 363

Depression, anxiety, repeated falls

Answer 364

International criteria: 1. Presence of dementia with 2 of: fluctuating attention and concentration, recurrent visual hallucinations, spontaneous parkinsonism. 2. If only 1 core feature, diagnosis can be made with a SPECT or PET scan showing low dopamine transporter uptake in basal ganglia

Answer 365

MMSE (mini mental state examination): score /30. >25 = normal. 18-25 = impaired. <18 = severely impaired. Tests communication, memory, activities of daily life. Bloods – FBC, U&Es, B12, LFTs (rule out other causes), urine MS+C for infection, brain MRI (generalised atrophy)

Answer 366

Parkinson’s disease, Alzheimer’s, frontotemporal dementia, vascular dementia

Answer 367

Supportive therapy: cognitive stimulation, exercise programmes, at-home care. Cholinesterase inhibitors e.g., donepezil, rivastigmine, to treat cognitive decline Avoid use of neuroleptic drugs, e.g., haloperidol

Answer 368

Pneumonia, institutionalisation, urinary incontinence

Answer 369

Seizures or convulsions caused by abnormal metabolic cirumstances, e.g. low Na+, hypoxia, and not due to epilepsy

Answer 370

VITAMIN DE: vascular, infection, trauma, autoimmune (e.g., SLE), metabolic (hypocalcaemia), idiopathic > epilepsy, neoplasms, dementia + drugs (cocaine), eclampsia + everything else.

Answer 371

Entirely situational e.g., metabolic disturbances, low Na+, hypoxia. Can be related syncope. Usually longer than epileptic seizures, with closed eyes and mouth Do not occur during sleep and do not involve incontinence or tongue-biting. Pre-ictal anxiety symptoms – they know they are about to happen

Answer 372

Impaired jerky movements, tunnel vision, paraesthesia, temporary blindness, palpitations, sweating, dry mouth, hyperventilation

Answer 373

Clinical diagnosis + normal EEG + normal CT/MRI

Answer 374

Blood tests for underlying cause

Answer 375

Psychotherapy/CBT. NES do not respond to anti-seizure medications

Answer 376

Lower back pain and symptoms associated with irritation of the sciatic nerve L4-S3

Answer 377

Spinal: IV disc herniation/prolapse, spinal stenosis, spondylolisthesis (anterior displacement of a vertebra out of line with the one below). Non-spinal: piriformis syndrome, tumours, pregnancy

Answer 378

Sciatic nerve (L4-S3) exits posterior pelvis through greater sciatic foramen and travels down the back of the leg. It divides at the knee to the tibial nerve and common peroneal nerve. It supplies sensation to lateral lower leg and foot. It supplies motor function to posterior thigh, lower leg and foot.

Answer 379

Unilateral pain from buttock down lateral leg to pinky toe. Weak plantar flexion and absent ankle jerk. Neurological deficit: leg weakness, sensory loss, bladder and bowel symptoms

Answer 380

Paraesthesia, numbness, motor weakness, reflexes affected

Answer 381

MRI spinal cord (signs of degeneration)

Answer 382

SOCRATES, Physical examination: can’t do straight leg raise test without pain (passive straight leg flexion with knee extended). Lumbar spine x-ray

Answer 383

Spinal tumour, spinal infection, spinal cord compression

Answer 384

1st line – NSAIDs (naproxen/ibuprofen/paracetamol) or Amitriptyline (TCA) or duloxetine (SNRI). Physiotherapy. Neurosurgery – nerve decompression

Answer 385

Facial pain in one or more distributions of the trigeminal nerve: ophthalmic, maxillary, mandibular. Usually unilateral

Answer 386

Increasing age, female, 20x more likely with multiple sclerosis

Answer 387

Compression of trigeminal nerve division

Answer 388

Triggers: eating, shaving, talking, brushing teeth, cold weather, spicy food, caffeine, citrus

Answer 389

Spontaneous facial electric shock pain (up to 2 mins) in V1/2/3. Paroxysms of sharp, stabbing, intense pain.

Answer 390

Clinical, 3 or more attacks with same presentation (paroxysmal sharp stabbing facial pain up to 2 mins)

Answer 391

MRI, trigeminal reflex testing, intra-oral testing

Answer 392

1st line – carbamazepine (anticonvulsant). Surgery to decompress nerve if nothing else works.

Answer 393

UMN lesion: lesion of the neural pathway above the anterior horn of the spinal cord or motor nuclei of the cranial nerves. LMN lesion: lesion which affects neural fibres travelling from the anterior horn of the spinal cord to the associated muscles.

Answer 394

UMN lesion: stroke, TIA, ALS, polio, cervical spine injury. LMN lesion: motor neuron disease, peripheral neuropathy, poliomyelitis, spinal cord injury with nerve root compression Mixed: multiple sclerosis, motor neuron disease

Answer 395

UMN: hypertonia, rigidity, spasticity. Hyperreflexia. No fasciculations. Babinski positive (stimulation of lateral foot leads to big toe extension). Power: Arms – flexors > extensors. Legs – flexors < extensors. LMN: hypotonia and muscle wasting. Hyporeflexia. Fasciculations. Babinski negative (stimulation of lateral foot does not cause big toe extension). Reduced power.

Answer 396

UMN: brain and spine MRI. LMN: electromyography and nerve conduction velocity tests.

Answer 397

Chronic progressive decline in cognitive function due to loss of brain parenchyma from cerebrovascular events such as infarction and small vessel changes

Answer 398

2nd most common dementia

Answer 399

Cerebrovascular damage from infarcts – TIA, stroke

Answer 400

Smoking, history of TIAs, atrial fibrillation, hypertension, T1DM, hyperlipidaemia, obesity, coronary heart disease

Answer 401

Stepwise progression: periods of stable symptoms, followed by sudden increase in severity. Visual disturbances, UMN signs (muscles weakness, hyperreflexia, clonus – involuntary rhythmic contractions), difficulty solving problems, apathy, disinhibition, poor attention, emotional disturbances, mood changes

Answer 402

Dementia diagnosis + sign of cerebrovascular event

Answer 403

History of TIA/stroke? Bloods to rule out cause: FBC, U&Es, LFT, B12, folate, TFTs. MMSE. Cognitive impairment screen: orientation, attention, language function, visuospatial functions, motor control CT/MRI – look for previous infarcts

Answer 404

Alzheimer’s, frontotemporal dementia, Lewy body dementia

Answer 405

1st line – antiplatelet therapy: aspirin or clopidogrel, or anticoagulation therapy: warfarin, rivaroxaban Supportive therapy and lifestyle changes SSRIs or antipsychotics to control symptoms, e.g., sertraline or lorazepam

Answer 406

Stroke, depression, agitation, wandering, falls

Answer 407

3-5 years from diagnosis

Answer 408

Radial nerve palsy (C5-T1) presenting as wrist drop

Answer 409

Radial nerve innervates extensor forearm muscles. Sensory to posterior forearm, lateral and dorsal aspect of hand, dorsal surface of the lateral 3.5 digits

Answer 410

Wrist drop, problems straightening arm at elbow, loss of sensation in dorsal hand and lateral 3.5 fingers.

Answer 411

Clinical exam + electromyography/nerve conduction studies

Answer 412

1st line – splint and simple analgesia

Neuro Flashcards

(436 cards)