Neuro Flashcards

Question 1

Q

Define haemorrhagic stroke

Answer

A

Rapid onset neurological deficit lasting over 24 hours caused by bleed in blood vessel in/around the brain, leading to infarction.
Two types: intracerebral haemorrhage and subarachnoid haemorrhage

Question 2

Q

Describe the epidemiology of haemorrhagic strokes

Answer

A

15% of strokes

Question 3

Q

Describe the aetiology for haemorrhagic stroke

Answer

A

Intracerebral haemorrhage, subarachnoid haemorrhage

Question 4

Q

Describe the risk factors for haemorrhagic strokes

Answer

A

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

Question 5

Q

Describe the pathophysiology for haemorrhagic stroke

Answer

A

Intracerebral haemorrhage: rupture of blood vessel within brain leading to oxygen deprivation and infarction. Pooling blood increased intracranial pressure
Subarachnoid haemorrhage: spontaneous bleeding into subarachnoid space between arachnoid mater and pia mater

Question 6

Q

What are the key presentations for haemorrhagic stroke

Answer

A

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

Question 7

Q

Describe the clinical manifestations for haemorrhagic strokes

Answer

A

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

Question 8

Q

What is the gold standard investigation for haemorrhagic stroke

Answer

A

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

Question 9

Q

Describe the first line investigations for haemorrhagic stroke

Answer

A

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

Question 10

Q

What are the differential diagnosis for haemorrhagic stroke

Answer

A

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

Question 11

Q

Describe the management for haemorrhagic stroke

Answer

A

1st line – confirm haemorrhagic on CT then neurosurgery referral.
Urgent lowering of blood pressure, IV mannitol to lower ICP, anticoagulation reversal

Question 12

Q

Describe the complications for haemorrhagic stroke

Answer

A

Infection, DVT, PE. seizures

Question 13

Q

Describe the prognosis for haemorrhagic strokes

Answer

A

40% mortality

Question 14

Q

Define ischaemic stroke

Answer

A

Rapid onset neurological deficit lasting over 24 hours due to a blood clot blocking blood supply to the brain, causing ischaemia and infarction.

Question 15

Q

Describe the epidemiology for ischaemic strokes

Answer

A

80% of strokes, older people, males, black/asian

Question 16

Q

Describe the aetiology for ischaemic strokes

Answer

A

Small vessel occlusion by thrombus, atherothromboembolism (e.g., from carotid artery), cardioembolism (from atrial fibrillation, MI, valve disease, infective endocarditis)
hyperviscosity, hypoperfusion, vasculitis, fat emboli from long bone fracture, venous sinus thrombus

Question 17

Q

Describe the risk factors for ischaemic strokes

Answer

A

Age, male, hypertension, smoking, diabetes, past TIA, hyperlipidaemia, heart disease (IHD, atrial fib, valve disease), combined oral contraceptive pill, peripheral arterial disease, clotting disorder

Question 18

Q

Describe the pathophysiology of ischaemic strokes

Answer

A

Blood vessel to/in brain is occluded by a clot causing ischaemia and infarction. Infarcted area dies causing focal neurological symptoms. Infarcted area is surrounded by oedema which can regain function with neurological recovery.

Question 19

Q

What are the key presentations for ischaemic strokes

Answer

A

Cerebral infarcts: Contralateral sensory loss, contralateral hemiplegia (initially flaccid, becomes spastic), UMN facial weakness (forehead sparing), dysphasia (speech), homonymous hemianopia, visuo-spatial deficit

Question 20

Q

Describe the clinical manifestations for ischaemic strokes

Answer

A

Signs: Brainstem infarcts: quadriplegia, facial numbness and paralysis, vision disturbances, dysarthria and speech impairment, vertigo, N+V
Cerebellar infarcts: palatal paralysis and diminished gag reflex, locked in syndrome, altered consciousness, coma
Lacunar infarcts (small perforating artery affecting internal capsule, basal ganglia, thalamus, pons): one of sensory loss, unilateral weakness, ataxic hemiparesis, dysarthria (motor speech problems)
Symptoms: Headache, nausea and vomiting, vertigo, decreased consciousness

Question 21

Q

What is the gold standard investigation for ischaemic stroke

Answer

A

Non-contrast CT scan (distinguishes ischaemic from haemorrhagic, shows site of infarct, identifies conditions mimicking a stroke)

Question 22

Q

Describe the first line investigations for ischaemic stroke

Answer

A

1st line: Urgent head CT/MRI. 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: Diffusion weighted MRI scan, carotid ultrasound

Question 23

Q

What are the differential diagnosis for ischaemic strokes

Answer

A

TIA, intracerebral haemorrhage, hypoglycaemia, complicated migraine, hypertensive encephalopathy

Question 24

Q

Describe the first line management for ischaemic strokes

Answer

A

1st line – haemorrhagic must be excluded. 300mg aspirin immediately after CT. Thrombolysis must happen within 4.5hours of symptoms: IV alteplase.
Other option: mechanical thrombectomy (endovascular removal of thrombus)
Antiplatelet therapy: aspirin 300mg daily for 2 weeks, then clopidogrel 75mg daily long term
Prophylaxis: atorvastatin, ramipril, anticoagulation (e.g., warfarin) for atrial fibrillation, carotid endarterectomy

Question 25

Q

Describe the complications for ischaemic stroke

Answer

A

Deep vein thrombosis, haemorrhagic transformation of ischaemic stroke

Question 26

Q

Describe the prognosis for ischaemic stroke

Answer

A

25% die within 1 year

Question 27

Q

Define transient ischaemic attack

Answer

A

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

Question 28

Q

Describe the epidemiology for TIA

Answer

A

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

Question 29

Q

Describe the aetiology for TIA

Answer

A

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

Question 30

Q

Describe the risk factors for TIA

Answer

A

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

Question 31

Q

Describe the pathophysiology for TIA

Answer

A

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

Question 32

Q

What are the key presentations for TIA

Answer

A

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

Question 33

Q

Describe the clinical manifestations for TIA

Answer

A

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

Question 34

Q

What is the gold standard investigation for TIA

Answer

A

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

Question 35

Q

Describe the first line investigations for TIA

Answer

A

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

Question 36

Q

What are the differential diagnosis for TIA

Answer

A

Stroke, hypoglycaemia, migraine aura, focal epilepsy, vasculitis

Question 37

Q

Describe the management for TIA

Answer

A

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

Question 38

Q

Describe the monitoring for TIA

Answer

A

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

Question 39

Q

What are the complications for TIA

Answer

A

Stroke, MI

Question 40

Q

Describe the prognosis for TIA

Answer

A

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

Question 41

Q

Define subarachnoid haemorrhage

Answer

A

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

Question 42

Q

Describe the epidemiology for subarachnoid haemorrhage

Answer

A

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

Question 43

Q

Describe the aetiology for subarachnoid haemorrhage

Answer

A

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.

Question 44

Q

Describe the risk factors for subarachnoid haemorrhage

Answer

A

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

Question 45

Q

Describe the pathophysiology for subarachnoid haemorrhage

Answer

A

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

Question 46

Q

What are the key presentations for subarachnoid haemorrhages

Answer

A

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)

Question 47

Q

Describe the clinical manifestations for subarachnoid haemorrhage

Answer

A

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.

Question 48

Q

What is the gold standard investigation for subarachnoid haemorrhage

Answer

A

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

Question 49

Q

What are the first line investigations for subarachnoid haemorrhage

Answer

A

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)

Question 50

Q

What are the differential diagnosis for subarachnoid haemorrhage

Answer

A

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

Question 51

Q

Describe the management for subarachnoid haemorrhage

Answer

A

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)

Question 52

Q

Describe the complications for subarachnoid haemorrhage

Answer

A

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

Question 53

Q

Describe the prognosis for subarachnoid haemorrhage

Answer

A

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

Question 54

Q

Define subdural haemorrhage

Answer

A

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

Question 55

Q

Describe the epidemiology for subdural haemorrhage

Answer

A

Babies (shaking baby syndrome), elderly, alcoholics

Question 56

Q

Describe the aetiology for subdural haemorrhage

Answer

A

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

Question 57

Q

Describe the risk factors for subdural haemorrhage

Answer

A

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

Question 58

Q

Describe the pathophysiology for subdural haemorrhage

Answer

A

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

Question 59

Q

What are the key presentations for subdural haemorrhage

Answer

A

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.

Question 60

Q

Describe the clinical manifestations for subdural haemorrhage

Answer

A

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

Question 61

Q

What is the gold standard investigation for subdural haemorrhage

Answer

A

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)

Question 62

Q

Describe the first line investigations for subdural haemorrhages

Answer

A

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

Other: MRI scan

Question 63

Q

What are the differential diagnosis for subdural haemorrhage

Answer

A

Epidural haematoma, intracerebral haematoma, stroke, seizure

Question 64

Q

Describe the management for subdural haemorrhage

Answer

A

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 65

A

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

Answer 66

A

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

Answer 67

A

Young people, males

Answer 68

A

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

Answer 69

A

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

Answer 70

A

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

Answer 71

A

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 72

A

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 73

A

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

Answer 74

A

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

Answer 75

A

Subdural haematoma, intracranial haematoma, subarachnoid haemorrhage, migraine

Answer 76

A

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

Answer 77

A

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

Answer 78

A

15% mortality

Answer 79

A

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

Answer 80

A

10% of strokes

Answer 81

A

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 82

A

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

Answer 83

A

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 84

A

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

Answer 85

A

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

Answer 86

A

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

Answer 87

A

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 88

A

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

Answer 89

A

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 90

A

Infection, deep vein thrombosis, pulmonary embolism, seizures

Answer 91

A

50% mortality

Answer 92

A

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 93

A

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

Answer 94

A

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

Answer 95

A

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

Answer 96

A

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 97

A

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 98

A

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 99

A

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

Answer 100

A

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 101

A

Syncope, TIA, generalised seizures, sleep disorders, chorea

Answer 102

A

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

Answer 103

A

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 104

A

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 105

A

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

Answer 106

A

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

Answer 107

A

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

Answer 108

A

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 109

A

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 110

A

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 111

A

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

Answer 112

A

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 113

A

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

Answer 114

A

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 115

A

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 116

A

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

Answer 117

A

Typically develops 55-65 years old

Answer 118

A

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 119

A

Age, male sex, pesticide exposure

Answer 120

A

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 121

A

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

Answer 122

A

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 123

A

Clinical diagnosis

Answer 124

A

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 125

A

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 126

A

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 127

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

Answer 128

A

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

Answer 129

A

Females, over 65

Answer 130

A

Beta-amyloid plaques, neurofibrillary tangles

Answer 131

A

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

Answer 132

A

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 133

A

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 134

A

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

Answer 135

A

Brain MRI (temporal lobe and cortical atrophy)

Answer 136

A

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 137

A

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

Answer 138

A

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 139

A

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

Answer 140

A

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

Answer 141

A

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

Answer 142

A

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

Answer 143

A

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

Answer 144

A

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 145

A

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 146

A

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 147

A

Clinical diagnosis

Answer 148

A

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 149

A

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

Answer 150

A

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 151

A

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

Answer 152

A

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 153

A

Stress, mental tension

Answer 154

A

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 155

A

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

Answer 156

A

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

Answer 157

A

Clinical diagnosis

Answer 158

A

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

Answer 159

A

Migraine, cluster headache, giant cell arteritis, sphenoid sinusitis

Answer 160

A

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 161

A

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

Answer 162

A

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 163

A

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

Answer 164

A

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

Answer 165

A

Hypothalamic activation with secondary trigeminal and autonomic activation.

Answer 166

A

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 167

A

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

Answer 168

A

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

Answer 169

A

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

Answer 170

A

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 171

A

Depression

Answer 172

A

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 173

A

Young females most common (20-40 years)

Answer 174

A

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

Answer 175

A

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

Answer 176

A

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 177

A

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 178

A

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 179

A

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 180

A

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 181

A

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

Answer 182

A

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 183

A

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

Answer 184

A

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 185

A

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

Answer 186

A

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

Answer 187

A

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 188

A

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 189

A

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 190

A

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 191

A

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

Answer 192

A

Myasthenia gravis, multifocal motor neuropathy, inclusion body myositis

Answer 193

A

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 194

A

Respiratory failure, aspiration pneumonia, swallowing failure, nutritional deficit

Answer 195

A

2-4 years post-diagnosis

Answer 196

A

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

Answer 197

A

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

Answer 198

A

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 199

A

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

Answer 200

A

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 201

A

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 202

A

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 203

A

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

Answer 204

A

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 205

A

Encephalitis, bacterial/viral/fungal/tuberculosis meningitis

Answer 206

A

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 207

A

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 208

A

20-30% mortality

Answer 209

A

Inflammation of brain parenchyma

Answer 210

A

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

Answer 211

A

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

Answer 212

A

Immunocompromised, extremes of age

Answer 213

A

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

Answer 214

A

Triad of fever, headache, altered mental status. Rash

Answer 215

A

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

Answer 216

A

MRI brain (swelling of brain)

Answer 217

A

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 218

A

Meningitis, encephalopathy, ischaemic stroke

Answer 219

A

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 220

A

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

Answer 221

A

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 222

A

Secondary brain tumours much more common

Answer 223

A

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

Answer 224

A

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 225

A

MRI head to locate tumour then biopsy to determine grade

Answer 226

A

No lumbar puncture due to raised ICP = massive contraindication

Answer 227

A

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

Answer 228

A

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

Answer 229

A

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

Answer 230

A

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

Answer 231

A

1st line – aspirin to prevent blood clots

Answer 232

A

Compression of the spinal cord from C1-L1/2

Answer 233

A

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 234

A

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 235

A

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 236

A

Paraplegia, back pain, paraesthesia, changes to tendon reflexes

Answer 237

A

MRI spine (visualise cord compression)

Answer 238

A

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

Answer 239

A

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

Answer 240

A

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

Answer 241

A

Pressure ulcers, autonomic dysfunction, DVT, falls

Answer 242

A

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

Answer 243

A

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

Answer 244

A

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 245

A

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 246

A

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

Answer 247

A

MRI spine (visualisation of lesion and nerve compression)

Answer 248

A

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 249

A

Spinal compression fracture, Guillain-Barre, transverse myelitis

Answer 250

A

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

Answer 251

A

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

Answer 252

A

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

Answer 253

A

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

Answer 254

A

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

Answer 255

A

Neurological examination, MRI

Answer 256

A

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

Answer 257

A

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

Answer 258

A

Females 40-60s, pregnant women

Answer 259

A

Swelling of carpal tunnel contents, narrowing of carpal tunnel

Answer 260

A

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

Answer 261

A

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 262

A

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 263

A

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

Answer 264

A

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

Answer 265

A

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 266

A

Osteoarthritis, ulnar neuropathy, polyneuropathy

Answer 267

A

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 268

A

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 269

A

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

Answer 270

A

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

Answer 271

A

Foot drop on clinical examination

Answer 272

A

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

Answer 273

A

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

Answer 274

A

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 275

A

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

Answer 276

A

Females (autoimmune), males (thymoma)

Answer 277

A

Family history, other autoimmune conditions, thymoma

Answer 278

A

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 279

A

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 280

A

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

Answer 281

A

Serology: acetylcholine receptors antibodies or muscle-specific kinase antibodies

Answer 282

A

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 283

A

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

Answer 284

A

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

Answer 285

A

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

Answer 286

A

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

Answer 287

A

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 288

A

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

Answer 289

A

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 290

A

Nerve conduction studies

Answer 291

A

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

Answer 292

A

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 293

A

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

Answer 294

A

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

Answer 295

A

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 296

A

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 297

A

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

Answer 298

A

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

Answer 299

A

Seizures, bradycardia, supraventricular tachycardias, ventricular tachycardias

Answer 300

A

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

Answer 301

A

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

Answer 302

A

Onset 30-50yo

Answer 303

A

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 304

A

Family history

Answer 305

A

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

Answer 306

A

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

Answer 307

A

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

Answer 308

A

Clinical diagnosis and genetic testing

Answer 309

A

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

Answer 310

A

SLE, Wilson’s disease, Sydenham’s chorea

Answer 311

A

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

Answer 312

A

Pneumonia, heart failure, MI, suicide

Answer 313

A

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

Answer 314

A

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

Answer 315

A

Males, peak ages 15-35 and 50-75

Answer 316

A

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

Answer 317

A

GI infection

Answer 318

A

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 319

A

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 320

A

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 321

A

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

Answer 322

A

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 323

A

Myasthenia gravis, Lambert-Eaton myasthenic syndrome, transverse myelitis

Answer 324

A

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

Answer 325

A

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

Answer 326

A

85% recover

Answer 327

A

Hemisection of the spinal cord. Mostly in cervical region

Answer 328

A

Penetrating trauma

Answer 329

A

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

Answer 330

A

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 331

A

MRI spine and neurological exam

Answer 332

A

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 333

A

Stroke, multiple sclerosis, transverse myelitis, hemiplegia

Answer 334

A

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

Answer 335

A

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

Answer 336

A

Childhood-adult onset

Answer 337

A

Autosomal dominant mutation

Answer 338

A

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 339

A

Nerve conduction studies, genetic testing

Answer 340

A

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

Answer 341

A

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

Answer 342

A

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 343

A

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

Answer 344

A

Clinical examination + electromyography/nerve conduction studies

Answer 345

A

1st line - splint and simple analgesia

Answer 346

A

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

Answer 347

A

20% of women, 12% of men

Answer 348

A

Combination of genetics, biological, environmental, psychological

Answer 349

A

Postnatal status, family history, dementia, stress

Answer 350

A

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

Answer 351

A

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 352

A

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 353

A

non-pharmacological: physical activity, healthy eating habits, psychotherapy/talk-therapy (CBT, interpersonal therapy)
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
electroconvulsive therapy (electrical induced seizures)

Answer 354

A

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

Answer 355

A

Young males, presents around 3yo

Answer 356

A

X-linked recessive

Answer 357

A

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 358

A

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 359

A

Genetic analysis

Answer 360

A

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

Answer 361

A

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

Answer 362

A

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

Answer 363

A

Wheelchair by 12, death by 30

Answer 364

A

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

Answer 365

A

Common dementia in under 65s

Answer 366

A

Neuron damage and death in frontal and temporal lobe, genetic

Answer 367

A

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

Answer 368

A

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

Answer 369

A

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 370

A

Brain MRI (temporal and frontal atrophy)

Answer 371

A

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 372

A

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

Answer 373

A

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 374

A

Financial crisis, dangerous driving, parenting problems

Answer 375

A

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

Answer 376

A

Autoimmune attack on presynaptic voltage gated calcium channels

Answer 377

A

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 378

A

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 379

A

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 380

A

Myasthenia gravis

Answer 381

A

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

Answer 382

A

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

Answer 383

A

Lewby bodies deposited in brain

Answer 384

A

Old age, family history

Answer 385

A

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 386

A

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 387

A

Depression, anxiety, repeated falls

Answer 388

A

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 389

A

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 390

A

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

Answer 391

A

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 392

A

Pneumonia, institutionalisation, urinary incontinence

Answer 393

A

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

Answer 394

A

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

Answer 395

A

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 396

A

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

Answer 397

A

Clinical diagnosis + normal EEG + normal CT/MRI

Answer 398

A

Blood tests for underlying cause

Answer 399

A

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

Answer 400

A

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

Answer 401

A

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 402

A

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 403

A

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 404

A

Paraesthesia, numbness, motor weakness, reflexes affected

Answer 405

A

MRI spinal cord (signs of degeneration)

Answer 406

A

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

Answer 407

A

Spinal tumour, spinal infection, spinal cord compression

Answer 408

A

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

Answer 409

A

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

Answer 410

A

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

Answer 411

A

Compression of trigeminal nerve division

Answer 412

A

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

Answer 413

A

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

Answer 414

A

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

Answer 415

A

MRI, trigeminal reflex testing, intra-oral testing

Answer 416

A

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

Answer 417

A

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 418

A

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 419

A

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 420

A

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

Answer 421

A

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

Answer 422

A

2nd most common dementia

Answer 423

A

Cerebrovascular damage from infarcts – TIA, stroke

Answer 424

A

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

Answer 425

A

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 426

A

Dementia diagnosis + sign of cerebrovascular event

Answer 427

A

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 428

A

Alzheimer’s, frontotemporal dementia, Lewy body dementia

Answer 429

A

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 430

A

Stroke, depression, agitation, wandering, falls

Answer 431

A

3-5 years from diagnosis

Answer 432

A

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

Answer 433

A

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 434

A

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

Answer 435

A

Clinical exam + electromyography/nerve conduction studies

Answer 436

A

1st line – splint and simple analgesia

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