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Medicine > Neurosciences > Flashcards

Neurosciences Flashcards

USMLE

1
Q

Define focal and generalised seizures

A

Focal seizures = Electrical discharge restricted to a limited part of the cortex of one cerebral hemisphere

Generalised seizures = Simultaneous involvement of both hemispheres, always associated with loss of consciousness

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2
Q

Give the three types of focal seizures

A

Aware
Impaired awareness
Focal to bilateral tonic-clonic seizure

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3
Q

Give localising features of focal seizures at frontal, temporal, parietal, and occipital lobes

A

Frontal
* Head/leg movements
* Posturing
* Jacksonian march (progressive clonic movements travelling from distal to proximal)
* Postictal Todd’s palsy
Temporal
* Aura
- rising epigastric sensation
- psychic/experiential phenomena, déjà vu, jamais vu
- hallucinations (auditory / gustatory / olfactory)
* Automatisms
* Seizures typically last around one minute
Parietal
* Paraesthesia/numbness
* Tingling
Occipital - Spots / lines / flashes

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4
Q

List the motor and non-motor onset seizures

A

Motor onset
* automatisms
* clonic
* tonic
* atonic
* epileptic spasms
* hyperkinetic
* myoclonic
Non-motor onset
* autonomic
* behavioural arrest
* cognitive
* emotional
* sensory

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5
Q

Give the first line management for seizures in community

A

Buccal midazolam

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6
Q

Give the first line management for focal seizures

A

Lamotrigine / levetiracetam

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7
Q

Give the first and second line managements for generalised seizures:
Absence seizures
Generalised tonic-clonic seizures
Myoclonic seizures
Tonic/atonic seizures

A

Absence seizures
1. ethosuximide
2. sodium valproate
Generalised tonic-clonic seizures
1. sodium valproate
2. lamotrigine / levetiracetam (women of childbearing age, girls)
Myoclonic seizures
1. sodium valproate
2. levetiracetam (women of childbearing age, girls)
Tonic/atonic seizures
1. sodium valproate
2. lamotrigine (women of childbearing age, girls)

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8
Q

Name two teratogenic effects associated with phenytoin

A

cleft palate
congenital heart disease

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9
Q

Give the clinical definition for epilepsy

A

Any of:
* At least two unprovoked seizures occurring > 24 hours apart
* One unprovoked seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years
* Diagnosis of epilepsy syndrome

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10
Q

Define psychogenic non-epileptic seizures

A

emotionally triggered attacks not associated with any paroxysmal epileptic activity in the brain

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11
Q

List the causes for epilepsy

A

(Only identified in ~⅓)

Structural
* Traumatic brain injury
* Hippocampal sclerosis
* Intracranial mass lesions
Vascular (most common cause of epilepsy in age > 60)
* Stroke
* Cavernous haemangiomas (cavernomas)
* Arteriovenous malformation
* Venous sinus thrombosis
Developmental - Cortical dysplasia
Primary generalised epilepsy - Juvenile myoclonic epilepsy
Genetic - Dravet syndrome
Infectious
* Viral encephalitis
* Meningitis
* Cerebral TB, malaria, toxoplasmosis
* HIV
* Neurocysticercosis
Metabolic abnormalities
* Hyponatraemia, hypocalcaemia, hypoglycaemia
* Acute hypoxia
* Porphyria
* Uraemia, hepatic encephalopathy
* Pyridoxine deficiency
Auto-immune CNS inflammation
* anti-NMDA receptor encephalitis
* anti-LG11 encephalitis

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12
Q

List the laboratory studies indicated for epileptic seizures

A

12-lead ECG - identify cardiac-related conditions that could mimic an epileptic seizure
Electrolyte panel (Na+, Mg2+, Ca2+)
Blood glucose
FBC - signs of systemic / CNS infection
Toxicology screen
Lumbar puncture - If fever / CNS infection suspected
EEG in all patients with suspected seizure
- focal cortical spikes or generalised spike-and-wave activity (in PGE)
Video/EEG long-term monitoring
Neuroimaging

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13
Q

Define status epilepticus

A

Prolonged convulsive seizure lasting for 5 minutes or longer, or recurrent seizures one after the other without recovery in between

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14
Q

List the causes for status epilepticus

A

Hypoxia
Trauma
Tumour
Stroke
Metabolic abnormalities
Drug/alcohol intoxication/withdrawal
Inadequate anticonvulsants in a known epileptic
Infection

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15
Q

Give managements for status epilepticus during the stages:
0 to 5 minutes: immediate management (stabilisation)
5 to 20 minutes: early status epilepticus
20 to 40 minutes: established status epilepticus
40 to 60 minutes: refractory status epilepticus

A

0 to 5 minutes: immediate management (stabilisation)
* Airway, Breathing, Circulation
* Give glucose if hypoglycaemia
* Thiamine (vitamine B1) before / at the same time as glucose if alcohol abuse or impaired nutrition
5 to 20 minutes: early status epilepticus
* IV lorazepam
20 to 40 minutes: established status epilepticus
* Second line IV anticonvulsant (levetiracetam / sodium valproate)
40 to 60 minutes: refractory status epilepticus
* Transfer to intensive care

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16
Q

Describe the characteristics of dysarthrias in:
Pseudobulbar palsy
Cerebellar lesions
Parkinson’s
Myasthenia gravis

A

Pseudobulbar palsy - gravelly speech
Cerebellar lesions - jerky ataxic speech
Parkinson’s - hypophonic monotone
Myasthenia gravis - fatigued speech, dies away

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17
Q

Locate the lesions on the optic tract:
(1) Mononuclear field loss
(2) Bitemporal hemianopia
(3) Homonymous hemianopia
(4) Superior homonymous quadrantanopia
(5) Inferior homonymous quadrantanopia
(6) Homonymous hemianopia with macular sparing
(7) Hemiscotoma

A

(1) Mononuclear field loss – complete optic nerve lesion.
(2) Bitemporal hemianopia – chiasmal lesion.
(3) Homonymous hemianopia – optic tract lesion.
(4) Superior homonymous quadrantanopia – temporal lesion (Meyer’s loop).
(5) Inferior homonymous quadrantanopia – parietal lesion.
(6) Homonymous hemianopia with macular sparing – occipital cortex or optic radiation.
(7) Hemiscotoma – occipital pole lesion.

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18
Q

List the triad in Horner syndrome

A

Partial ptosis
Unilateral miosis
Facial anhidrosis

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19
Q

List the causes of Horner syndrome

A

(Damage to sympathetic nervous supply to the eye)

Hypothalamus - infarction
Brainstem
* Brainstem demyelination
* Lateral medullary infarction
Cervical cord
* Syringomyelia
* Tumours
T1 root
* Apical lung tumour
* Tuberculosis
* Cervical rib trauma
* Brachial plexus trauma
Sympathetic chain and carotid artery
* Thyroid/laryngeal/carotid surgery
* Carotid artery dissection
* Neoplastic infiltration
* Cervical sympathectomy

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20
Q

Locate the lesion and list the causes when there is:
Anhidrosis of the face, arm and trunk
Anhidrosis of the face
No anhidrosis

A

Central lesions: anhidrosis of the face, arm and trunk
* Stroke
* Syringomyelia
* Multiple sclerosis
* Tumour
* Encephalitis
Preganglionic lesions: anhidrosis of the face
* Pancoast’s tumour
* Thyroidectomy
* Trauma
* Cervical rib
Postganglionic lesions: No anhidrosis
* Carotid artery dissection
* Carotid aneurysm
* Cavernous sinus thrombosis
* Cluster headache

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21
Q

Where does the vestibular schwannoma develop from

A

Develops from the vestibular divisions of the vestibulocochlear nerve within the internal auditory canal

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22
Q

List the presentations for vestibular schwannoma

A

Progressive unilateral sensorineural hearing loss
Tinnitus
Intermittent dizziness
Vertigo

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23
Q

List the causes for cerebellar syndromes

A

Tumours
* Hemangioblastoma
* Medulloblastoma
* Metastasis
* Compression by vestibular schwannoma
Vascular
* Haemorrhage/Infarction
* Arteriovenous malformation
Infection
* Abscess
* HIV
* Prion diseases
* Encephalitis
Developmental
* Arnold–Chiari malformation
* Cerebral palsy
Toxic and metabolic
* Antiepileptic drugs
* Chronic alcohol use
* Carbon monoxide poisoning
* Lead poisoning
* Solvent misuse
Inherited
* Friedreich’s and other spinocerebellar ataxias
* Ataxia telangiectasia
Others
* Multiple sclerosis
* Hydrocephalus
* Hypothyroidism
* Paraneoplastic syndromes (rapidly progressive)
* Multiple system atrophy

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24
Q

List the presentations by lateral cerebellar hemisphere lesions

A

Broad, ataxic gait faltering towards the side of the lesion
Rebound upward overshoot when the limb is pressed downwards and released
Dysmetria, dysdiadochokinesia
Intention tremor
Preserved speed of fine movement
Coarse horizontal nystagmus, the fast component is always towards the side of the lesion
Scanning dysarthria
Titubation
Hypotonia
Slow, pendular reflexes

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25
Q

List the presentations by cerebellar vermis lesions

A

Truncal ataxia (difficulty standing and sitting unsupported)
Broad-based, ataxic gait

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26
Q

List the presentations by Flocculonodular region lesions

A

Vertigo and vomiting
Gait ataxia

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27
Q

List the causes for an ischaemic stroke (85% cases)

A

Thrombus (atherosclerosis)
Embolus (atrial fibrillation, atherosclerosis of the carotid arteries)
Intra/extracranial vessels diseases:
* Carotid artery dissection
* Vasculitis
* Cerebral venous thrombosis
Haematological condition:
* Sickle cell anaemia
* Antiphospholipid syndrome

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28
Q

List the causes for an haemorrhagic stroke (15% cases)

A

Intracerebral haemorrhage - Hypertension
Subarachnoid haemorrhage
* Intracranial aneurysm rupture
* Arteriovenous malformations
* Arterial dissections
* Anticoagulant use

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29
Q

List the complications in the early period following stroke

A

Hemorrhagic transformation of ischaemic stroke
Cerebral oedema
Delirium
Seizures
Pulmonary embolism
Cardiac complications
* Myocardial ischemia
* Congestive heart failure
* Atrial fibrillation
* Arrhythmias
Infection
* Aspiration pneumonia
* Urinary tract infection
* Cellulitis from infected pressure sores

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30
Q

Describe the presentations of a TIA

A

Neurological dysfunction < 24 hours
Unilateral weakness/sensory loss
Dysphasia
Ataxia, vertigo, loss of balance
Syncope
Amaurosis fugax, diplopia, homonymous hemianopia
Cranial nerve deficits

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31
Q

List the risk factors for stroke

A

Lifestyle factors
* Smoking.
* Alcohol misuse and drug abuse (cocaine, methamphetamine).
* Physical inactivity.
* Poor diet.
Cardiovascular diseases:
* Hypertension
* Atrial fibrillation
* Infective endocarditis
* Valvular disease
* Carotid artery disease
* Congestive heart failure
* History of myocardial infarction
* Congenital / structural heart disease
Other medical conditions:
* Migraine.
* Hyperlipidaemia.
* Diabetes mellitus.
* Sickle cell disease.
* Haemophilia.
* Antiphospholipid syndrome and other hypercoagulable disorders.
* Chronic kidney disease.
* Ehlers-Danlos syndrome.
* Marfan syndrome.
* Pseudoxanthoma elasticum.
* Polycystic kidney disease.
* Neurofibromatosis type I.
* Obstructive sleep apnoea.
* Vascular malformations
Other factors:
* Older age
* Gender
Male sex - more likely to have a stroke at a younger age
Female sex
* Anticoagulation
* Previous TIA/stroke, family history of stroke

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32
Q

What increases the risk of stroke in female population

A

Combined oral contraceptives
Immediate postpartum period
Pre-eclampsia

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33
Q

List 4 risk factors for cerebral venous thrombosis

A

Pregnancy
Infection
Dehydration
Malignancy

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34
Q

List the components of the Glasgow Coma Scale

A

Best motor response
6 - obeys commands
5 - localising pain
4 - withdrawal from pain
3 - flexion to pain
2- extension to pain
1 - no motor response
Best verbal response
5 - oriented
4 - confused
3 - inappropriate words
2 - incomprehensible sounds
1 - no verbal response
Best eye response
4 - open spontaneously
3 - open to verbal command
2 - open to pain
1 - no eye opening

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35
Q

List the immediate examinations performed in stroke

A

The level of consciousness using Glasgow Coma Scale
Airway, breathing, and circulation
Vital signs
* Blood pressure
* Heart rate
* Respiratory rate
* Oxygen saturation
* Temperature
Focused neurological examination - Face Arm Speech Test (FAST)
The cardiovascular system
* Arrhythmia (atrial fibrillation)
* Murmurs
* Pulmonary oedema
* Heart failure

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36
Q

Give the immediate management of a suspected TIA

A

Aspirin 300 mg immediately
* PPI cover if dyspepsia
* Clopidogrel if aspirin contraindicated

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37
Q

Give the management for secondary prevention of stroke

A

No AF - Antiplatelet therapy
* clopidogrel 75 mg
* Intolerance - Aspirin 75 mg daily with modified-release dipyridamole 200 mg twice daily
AF - Anticoagulant drugs
* Valvular AF - Adjusted-dose warfarin
* Non-valvular AF - Direct thrombin (Dabigatran) / factor Xa inhibitor (Apixaban, Betrixaban, Edoxaban, Rivaroxaban)
High-intensity statin - Atorvastatin 20-80 mg daily
Antihypertensive drugs

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38
Q

In which patients non-contrast head CT should be performed within 1 hour?

A

To exclude intracranial haemorrhage:
Indicated for thrombolysis or thrombectomy
On anticoagulant treatment
Known bleeding tendency
Depressed level of consciousness (GCS scale score <13)
Unexplained progressive / fluctuating symptoms
Papilloedema, neck stiffness, fever
Severe headache at onset of stroke symptoms
Uncertain diagnosis

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39
Q

Give features on a non-contrast CT head for an ischaemic stroke

A

hypoattenuation (darkness) of the brain parenchyma
loss of grey-white matter differentiation, sulcal effacement
hyperattenuation (brightness) in an artery indicates clot

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40
Q

What laboratory studies should be indicated in an ischaemic stroke

A

Serum glucose - hypo/hyperglycaemia (before thrombolysis)
Serum electrolytes - electrolyte disturbance
Serum urea and creatinine - renal failure
Cardiac enzymes - concomitant myocardial infarction
ECG - cardiac arrhythmia/ischaemia
FBC - anaemia/thrombocytopenia before thrombolysis, anticoagulants, or antithrombotics.
PT and aPTT (with INR) - coagulopathy.

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41
Q

Give the managements in an ischaemic stroke

A

IV alteplase / tenecteplase within 4.5 hours of known onset

Manage ABC
* Endotracheal intubation if unable to protect their airway or GCS score ≤8
* Supplemental oxygen if sat < 93%

Mechanical thrombectomy if confirmed occlusion of the proximal anterior circulation (ICA/M1) or the proximal posterior circulation (basilar/PCA).

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42
Q

Give the most common cause of intracerebral haemorrhage

A

Chronic hypertension resulting in
* Rupture of microaneurysms (Charcot–Bouchard aneurysms)
* Degeneration of small, deep, penetrating arteries

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43
Q

List the Nonhypertensive Causes of Intracerebral Haemorrhage

A

Cerebral amyloid angiopathy
Vascular malformations
* Saccular/mycotic aneurysms
* Arteriovenous malformations
* Cavernous angiomas
* Moyamoya disease
Intracranial tumours
Bleeding disorders, anticoagulant and fibrinolytic treatment
Vasculitides
* Granulomatous angiitis of the central nervous system
* Polyarteritis nodosa
Sympathomimetic agents
* Amphetamine
* Cocaine
Hemorrhagic infarction
Head trauma
Septic emboli/arteritis in the setting of infective endocarditis

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44
Q

Give the non-contrast CT imaging features for an intracerebral haemorrhage

A

hyperattenuation (brightness), suggesting acute blood, often with surrounding hypoattenuation (darkness) due to oedema

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45
Q

List 4 causes for a nontraumatic subarachnoid haemorrhage

A

Aneurysm rupture (80%)
Arteriovenous malformations
Arterial dissections
Anticoagulant use

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46
Q

List the symptoms for a subarachnoid haemorrhage

A

Thunderclap headache
Neck stiffness
Nausea and Vomiting
Photophobia
Loss of consciousness
Seizures (7%)
Diplopia (CN VI), eyelid drooping, mydriasis, orbital pain (CN III)
Visual loss (Intraocular haemorrhage from increased ICP)
Agitation
Focal neurological deficits
* Unilateral loss of motor function
* Loss of visual field
* Aphasia

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47
Q

Give the non-contrast CT imaging features for a subarachnoid haemorrhage

A

Presence of hyperdense appearance of blood in the subarachnoid space / basal cisterns

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48
Q

List two differentials for a sudden onset of severe headache and an elevated CSF opening pressure

A

cerebral venous sinus thrombosis
idiopathic intracranial hypertension

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49
Q

What may a sudden onset of severe headache and a reduced CSF opening pressure suggest

A

low pressure headache

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50
Q

List two cardiac complications from an aneurysm rupture

A

Left ventricular subendocardial injury
Takotsubo cardiomyopathy

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51
Q

List the investigations and findings after a subarachnoid haemorrhage

A

Full blood count - Leukocytosis (independent risk factor for cerebral vasospasm)
Serum electrolytes - Hyponatremia (associated with SIADH)
Serum glucose - Hyperglycemia (Present in ⅓. Feature of any acute brain injury)
Clotting profile - coagulopathy (elevated INR, prolonged PTT)
Serum troponin I - Elevated (acute myocardial injury due to autonomic dysregulation with sympathetic stimulation)
ECG
* Arrhythmias and ischaemic changes
* Prolonged QT
* ST segment / T wave abnormalities

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52
Q

Give the immediate medical management for SAH

A

Oral nimodipine

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53
Q

List the management approaches towards an intracerebral haemorrhage

A

IV mannitol - reduce ICP
Stop / reverse anticoagulation
BP control < 140 mmHg systolic
Surgical eg. EVD

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54
Q

List the signs of rebleeding after SAH

A

Sudden drop in conscious level
Spike in blood pressure
Tonic/extensor posturing
Pupillary changes

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55
Q

List the management approaches for rebleeding after SAH

A

Early aneurysm repair
Short-term Tranexamic acid

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56
Q

What are the short term complications after SAH

A

Rebleeding
Acute hydrocephalus
Seizures
Vasospasm and delayed cerebral ischaemia

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57
Q

Give signs of an acute hydrocephalus after SAH

A

A gradually worsening level of arousal with relative preservation of deliberate motor responses
Severe headache/vomiting/agitation

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58
Q

Give a management approach for acute hydrocephalus after SAH

A

CSF drainage or diversion

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59
Q

Give signs for a vasospasm and delayed cerebral ischaemia after SAH

A

≥ 2 drop in GCS score
New focal neurological deficit (e.g., unilateral motor or sensory loss, speech disturbance, visual field loss)

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60
Q

List the management approaches in vasospasm and delayed cerebral ischaemia after SAH

A

Triple-H (uses hypertension, hypervolaemia, and haemodilution)
Endovascular strategies (balloon angioplasty / intra-arterial vasodilators)

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61
Q

List the risk factors for cerebral aneurysms

A

Hereditary connective tissue diseases:
* ADPKD
* Neurofibromatosis type 1
* Ehlers-Danlos syndrome type IV
* Marfan’s syndrome
Hypertension
Arteriovenous malformations/fistulas
Smoking, Alcohol, Drug abuse

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62
Q

List the causes for subdural haematoma

A

Trauma (most common)
Rupture of a cerebral aneurysm
Vascular malformation
* AVM
* Dural fistula

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63
Q

What does acute SDH typically result from?

A

torsional / shear forces causing disruption of bridging cortical veins

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64
Q

List the CT appearances in SDH

A

Acute - <3 days old, diffusely hyperdense
Subacute - 3~21 days old, heterogeneously hyperdense/isodense
Chronic - >21 days old, diffusely hypodense
Acute-on-chronic - areas of hyperdensity within hypodense haematoma

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65
Q

List the signs of a skull base fracture

A

Raccoon eyes
CSF rhinorrhea
CSF otorrhea
Haemotympanum

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66
Q

Give the typical time line in extradural haemorrhage

A

Head injury with a brief duration of unconsciousness
Followed by improvement (lucid interval)
Then becomes stuporose
* Ipsilateral dilated pupil
* Contralateral hemiparesis
* Transtentorial coning
Followed by
* Bilateral fixed, dilated pupils
* Tetraplegia
* Respiratory arrest

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67
Q

List the differential diagnoses for dementia syndrome

A

Normal-age related memory changes
Mild cognitive impairment
Depression
Delirium
Thiamine deficiency (Wernicke-Korsakoff’s syndrome)
Hypothyroidism
Normal pressure hydrocephalus

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68
Q

List the risk factors for dementia syndrome

A

Age
Mild cognitive impairment (MCI)
Learning disability
Genetics
Cardiovascular disease
Cerebrovascular disease
Parkinson’s disease (PD)

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69
Q

List the causes for dementia syndrome

A

Alzheimer’s disease (50–75% of cases)
Vascular dementia (up to 20% of cases)
Dementia with Lewy bodies (DLB) (10–15% of cases)
Frontotemporal dementia (FTD) (2% of cases)

Other causes of dementia:
Parkinson’s disease (PD) dementia
Progressive supranuclear palsy
Huntington’s disease
Cretzfeldt-Jakob disease (Prion disease)
Normal pressure hydrocephalus
Chronic subdural haematoma
Benign tumours
Metabolic and endocrine disorders
* Chronic hypothyroidism
* Addison’s disease
* Hypopituitarism
Vitamin deficiencies (B12, thiamine)
Infections (HIV, syphilis)
Inflammatory and autoimmune disorders
Transient epileptic amnesia

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70
Q

Name two pathological findings in Alzheimer’s disease

A

extracellular plaques composed primarily of amyloid
intraneuronal neurofibrillary tangles composed primarily of hyperphosphorylated tau

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71
Q

List the specific features for Alzheimer’s disease

A

Loss of recent memory first
Difficulty with executive function / nominal dysphasia
Loss of episodic memory
Cognitive deficits - aphasia, apraxia, agnosia

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72
Q

List the management for Alzheimer’s disease

A

Acetylcholinesterase (AChE) inhibitors - mild to moderate AD
* Donepezil
* Rivastigmine
* Galantamine
Memantine (N-methyl-D-aspartic acid receptor antagonist) - moderate to severe AD

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73
Q

List the causes for vascular dementia

A

Large / multiple small infarcts
Haemorrhage
Cerebral amyloid angiopathy
Subcortical leukoencephalopathy

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74
Q

List the specific features in vascular dementia

A

Stepwise increase in severity of symptoms

Focal neurological signs eg. hemiparesis / visual field defects

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75
Q

List the specific features for Dementia with Lewy Bodies

A

REM sleep behaviour disorder
Fluctuating cognition
Recurrent visual hallucinations
One or more symptoms of Parkinsonism - bradykinesia, rest tremor, rigidity, postural instability
Memory impairment in later stages

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76
Q

Give the first line management in Dementia with Lewy Bodies

A

donepezil or rivastigmine

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77
Q

List four conditions which Frontotemporal dementia maybe associated with

A

Amyotrophic lateral sclerosis (ALS)
Parkinsonism
Corticobasal degeneration
Progressive supranuclear palsy

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78
Q

What drugs should FTD not be offered with

A

AChEi
Memantine

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79
Q

List the diagnostic criteria for delirium

A

Evident disturbance in attention
Cognitive change
Develops over a short period of time
Evident physiological disturbance

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80
Q

Give three clinical subtypes of delirium

A

Hyperactive
Hypoactive
Mixed

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81
Q

List the common causes of delirium

A

PINCHME:

Pain
Infection
Nutrition
Constipation
deHydration
Medication
Environment

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82
Q

Give the pathophysiology of migraine

A

Headache of migraine results from neurogenic inflammation of CNV1 sensory neurons (Innervates the large vessels and meninges of the brain)
CNV neurons release substances that cause dilation of the meningeal blood vessels, leakage of plasma proteins into surrounding tissues, and platelet activation.
This peripheral sensitisation results in increased nociceptive inputs into CNV sensory nucleus and ultimately central sensitisation. Therefore, non-painful stimuli (eg. light touch) are interpreted as pain.

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83
Q

Give key features of migraine

A

Intermittent Headache
Visual disturbance
Nausea and vomiting
Photophobia and phonophobia
Reduced ability to function

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84
Q

List the management approaches to migraine

A

aspirin (900 mg)
sumatriptan

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85
Q

List the medication for prophylaxis in migraine

A

propanolol

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86
Q

List the triggers for tension type headache

A

Psychological stress (most common)
Disturbed sleep patterns (episodic)
Insomnia and other sleep disorders (chronic)

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87
Q

Describe the clinical features in tension headache

A

Dull, non-pulsatile pain (typically expressed as being a ‘tight band’ around the head)

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88
Q

list the medication for an acute attack of tension headache

A

Aspirin

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89
Q

What may cluster headache be precipitated by?

A

Alcohol
Volatile smells
Warm temperatures
Sleep

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90
Q

List three cardinal features in cluster headache

A

Trigeminal distribution of the pain
Ipsilateral cranial autonomic symptoms
Circadian/circannual pattern of attacks

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91
Q

Give the International Headache Society (IHS) diagnostic criteria for cluster headache

A

Severe unilateral orbital, supra-orbital, and/or temporal pain lasting 15 to 180 minutes
At least one of the following symptoms or signs, ipsilateral to the headache:
* Conjunctival injection, lacrimation
* Nasal congestion, Rhinorrhoea
* Eyelid oedema, Facial and forehead sweating
* Miosis, Ptosis
* Sense of restlessness or agitation.

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92
Q

Give the acute attack therapy in cluster headaches

A

subcutaneous sumatriptan / nasal zolmitriptan
High flow oxygen

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93
Q

Give the preventative therapy in cluster headaches

A

Verapamil

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94
Q

Give the symptom in trigeminal neuralgia

A

Unilateral paroxysms of facial pain lasting seconds to minutes in a distribution along ≥1 divisions of the CNV

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95
Q

Describe the pathophysiology in trigeminal neuralgia

A

Neuropathic pain due to focal demyelination and resultant conduction aberration

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96
Q

List the triggers for trigeminal neuralgia

A

Tooth brushing
Eating
Cold
Touch

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97
Q

Give the medical management in trigeminal neuralgia

A

Carbamazepine
Oxcarbazepine

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98
Q

Give one complications for giant cell arteritis

A

irreversible vision loss due to optic nerve ischaemia

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99
Q

List the presentations in giant cell arteritis

A

Age >50 yrs
New onset headache
Limb, jaw, tongue claudication
Scalp tenderness
Acute visual symptoms (amaurosis fugax)
Unexplained raised ESR/CRP
Constitutional symptoms:
* Fever
* Fatigue
* Night sweats
* Weight loss

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100
Q

Give the medical management in giant cell arteritis

A

IV high-dose methylprednisolone

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101
Q

Give the histological features in giant cell arteritis

A

Granulomatous inflammation of the intima and media
Breaking up of the internal elastic lamina
Giant cells, lymphocytes and plasma cells in the internal elastic lamina

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102
Q

List the spinal reflex arcs and their levels

A

S1-2 Ankle
L3-4 Knee jerk
C5-6 Biceps
C7-8 Triceps

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103
Q

Describe the patterns of sensory loss in the following lesions

(A) Thalamic lesion (rare)
(B) Brainstem lesion
(C) Central cord lesion
(D) Hemisection of cord/unilateral cord lesion
(E) Transverse cord lesion
(F) Dorsal column lesion
(G) Individual sensory root lesions
(H) Polyneuropathy

A

(A) Thalamic - sensory loss throughout the opposite side.
(B) Brainstem - contralateral sensory loss below face and ipsilateral loss on face.
(C) Central cord - ‘suspended’ areas of loss, often asymmetrical and ‘dissociated’: i.e. pain and temperature lost but light touch intact.
syrinx
(D) Hemisection of cord/unilateral cord lesion - Brown–Séquard syndrome: contralateral spinothalamic (pain and temperature) loss with ipsilateral weakness and dorsal column loss below lesion.
(E) Transverse cord - loss of all modalities, including motor, below lesion.
(F) Dorsal column - loss of proprioception, vibration and light touch. (multiple sclerosis)
(G) Individual sensory root lesions, e.g. C6, T5, L4.
(H) Polyneuropathy - distal sensory loss. UMN, upper motor neuron.

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104
Q

List the presentations in central cord syndromes

A

Weakness in the upper extremities greater than the lower
Pain and temperature loss 2/3 levels caudal to the lesion
Loss of bladder control
If lesion expands:
* bilateral spastic paraparesis of the lower extremities
* asymmetric upper extremity paraparesis

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105
Q

List the presentations in anterior cord syndromes

A

(Involve the anterior two-thirds of the spinal cord)
Pain, temperature, and motor function below the level of the lesion lost
Vibration, proprioception, and fine touch sensation intact

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106
Q

List the presentations in posterior column syndrome

A

Loss of vibration and proprioception
Spastic paraparesis and brisk reflexes
Urgency and incontinence
Retained pain and temperature sensation

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107
Q

List the presentations in syringomyelia

A

‘Suspended’ area of dissociated sensory loss (cape like distribution)
Loss of upper limb reflexes
Hand and forearm muscle wasting
Spastic paraparesis (initially mild)
Brainstem signs (syringobulbia)
* Tongue atrophy and fasciculation
* Bulbar palsy
* Horner’s syndrome
* Impairment of facial sensation

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108
Q

List the causes for spinal cord compression

A

Spinal cord tumours
* Extramedullary - meningioma, neurofibroma
* Intramedullary - ependymoma, glioma
Bony metastases (vertebral body destruction)
Disc and vertebral lesions:
* Chronic degenerative
* Acute central disc prolapse
* Trauma
Inflammatory:
* Epidural abscess
* Tuberculosis
* Granulomatous
Epidural haemorrhage / haematoma

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109
Q

List the signs for cervical spondylotic radiculopathy

A

Radiating arm pain
Mild weakness in the muscles
Reflex changes

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110
Q

List the signs for degenerative cervical myelopathy

A

Loss of hand coordination
Hand intrinsic muscles weakness eg. interossei
Mild gait ataxia (impaired position sense)
Bowel and bladder difficulties in severe cases

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111
Q

List the metastatic causes for malignant spinal cord compression

A

Prostate
Breast
Lung
Renal
Thyroid

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112
Q

List the lab tests ordered in malignant spinal cord compression

A

serum calcium levels - hypercalcaemia
serum ALP - elevated
cancer-specific laboratory testing
* prostate specific antigen (PSA)
* breast cancer genes 1 and 2 (BRCA1 and 2)
* carcinoembryonic antigen (CEA)
* serum and urine protein electrophoresis

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113
Q

List the afferent and efferent pupillary light reflex pathway

A

Afferent pathway:
1. Light activates optic nerve axons.
2. Axons (some decussating at the chiasm) pass through each lateral geniculate body
3. Synapse at pretectal nuclei.
Efferent pathway:
4. Action potentials pass to Edinger–Westphal nuclei of the CN III
5. Via parasympathetic neurons in CN III to cause
6. Pupil constriction

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114
Q

List the signs of a left APD

A

Absent direct and consensual reflex
Intact consensual reflex of the right eye

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115
Q

What does an incomplete damage to one optic nerve relative to the other cause?

A

Relative afferent pupillary defect

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116
Q

What is internuclear ophthalmoplegia caused by

A

lesion of the medial longitudinal fasciculus

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117
Q

List the major cause of internuclear ophthalmoplegia

A

Multiple sclerosis

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118
Q

List the signs of internuclear ophthalmoplegia

A

Ipsilesional adduction deficit
Contralateral, horizontal abducting nystagmus on attempted gaze to the contralesional side

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119
Q

List the signs of large vestibular schwannoma

A

Headache
CN5 compression
* Hemifacial hypo/paraesthesia
* Trigeminal neuralgia
CN7 compression - Facial spasm/weakness
4th ventricle compression - Obstructive hydrocephalus
Cerebellar displacement
* Nystagmus
* Ataxia

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120
Q

List the central and peripheral causes of vertigo

A

Peripheral
* Benign paroxysmal positional vertigo
* Meniere’s disease
* Labyrinthitis
* Labyrinthine concussion
* Vestibular neuronitis
* Vestibular ototoxicity
* Perilymphatic fistula
* Semicircular canal dehiscence syndrome
* Syphilis

Central
* Migraine
* Stroke
* Cerebellar tumour
* Vestibular schwannoma
* Multiple sclerosis

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121
Q

List the vestibular migraine features

A

vertigo
visual disorders
occipital pressure
nausea and vomiting

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122
Q

Give the major mechanisms of all subtypes of BPPV

A

Canalithiasis

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123
Q

Give the major mechanism of lateral canal BPPV

A

Cupulolithiasis

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124
Q

List the secondary causes of BPPV

A

Head trauma
Labyrinthitis
Vestibular neuronitis
Meniere’s disease (endolymphatic hydrops)
Migraines
Ischaemia
Iatrogenic

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125
Q

List the subtypes of BPPV

A

Posterior canal
Lateral canal
Superior canal

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126
Q

Give the presentation of BPPV

A

Sensation that the environment is spinning around relative to oneself
Sudden onset and intense vertigo
Precipitated by head movements
Short duration
Episodic and recurrent

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127
Q

What does the Dix-Hallpike manoeuvre test for?

A

Posterior canal BPPV

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128
Q

Describe the Dix-Hallpike manoeuvre

A
  1. The patient sits on the examination table
  2. their head is turned 45° to one side
  3. then they are laid back into a supine position, with the head hanging back but supported by the examiner and the neck extended by about 30°
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129
Q

Describe the Dix-Hallpike manoeuvre findings in right sided BPPV

A

Eyes rotate in an anticlockwise manner during the fast phase of nystagmus
With a slight up-beating vertical component (towards the forehead)

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130
Q

Describe the Dix-Hallpike manoeuvre findings in left sided BPPV

A

Eyes rotate in a clockwise manner during the fast phase of nystagmus
With a slight up-beating vertical component (towards the forehead)

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131
Q

What does supine lateral head turns test for

A

lateral canal BPPV

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132
Q

Give the hallmark feature in lateral canal BPPV, when tested by supine lateral head turns

A

pure horizontal nystagmus without a torsional (rotatory) component

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133
Q

List the signs of canalithiasis, when tested by supine lateral head turns

A

horizontal nystagmus with the fast phase beating towards the ground (geotropic)
the side with the stronger response is the affected side

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134
Q

List the signs of cupulolithiasis, when tested by supine lateral head turns

A

the fast phase beats away from the ground (apogeotropic)
the side with the weaker response is the affected side

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135
Q

Give the management for BPPV

A

Particle repositioning manoeuvre

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136
Q

Define Meniere’s disease

A

Endolymphatic hydrops - overproduction or impaired absorption of endolymph

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137
Q

Give the classic presentation in Meniere’s disease

A

Episodic sudden onset of vertigo, hearing loss, tinnitus, and sensation of fullness in the affected ear.

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138
Q

List the signs in Meniere’s disease

A

Positive Romberg’s test
Inability to walk tandem (heel to toe) in a straight line
Fukuda stepping test (march in place with eyes closed) - unable to maintain position and turn towards the affected side

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139
Q

List the management options in Meniere’s disease

A

Salt restriction to 1500~2300 mg/day - prevent Na+ related water retention and re-distribution into the endolymphatic system
Thiazide diuretics
Lifestyle:
* Limit caffeine
* Reduce alcohol
* Ceasing smoking
* Managing stress

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140
Q

Define Labyrinthitis

A

Inflammation of the otic capsule:
* Cochlea
* Three orthogonal semi-circular canals
* Otolith organs (utricle, saccule)

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141
Q

What does suppurative (bacterial) labyrinthitis present with

A

severe to profound hearing loss (typically irreversible) and vertigo

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142
Q

What is suppurative (bacterial) labyrinthitis associated with?

A

(Direct microbial invasion of the inner ear)
Acute/chronic otitis media
Cholesteatoma
Meningitis

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143
Q

List the potential bacterial causes in suppurative (bacterial) labyrinthitis

A

Treponema pallidum
Haemophilus influenzae
Streptococcus species
Staphylococcus species
Neisseria meningitidis

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144
Q

What does serous (viral) labyrinthitis present with

A

less severe hearing loss (often reversible) and vertigo than suppurative labyrinthitis.

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145
Q

Is suppurative (bacterial) labyrinthitis more common in adults or children

A

adults

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146
Q

What is serous (viral) labyrinthitis associated with

A

Preceding URTI
Autoimmune inner ear disease
* Cogan’s syndrome
* Behçet’s disease

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147
Q

List the viral agents involved in serous (viral) labyrinthitis

A

Varicella zoster virus
Cytomegalovirus
Mumps, measles, rubella
HIV

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148
Q

List the presentations in labyrinthitis

A

Unilateral sensorineural hearing loss
Tinnitus
Vertigo with nausea and vomiting

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149
Q

List the signs in labyrinthitis

A

Spontaneous horizontal-rotary nystagmus - fast phase beating towards the normal ear
Significant difficulty walking
Unable to perform tandem gait
Fall with Romberg’s testing

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150
Q

List the causes of vestibular neuronitis

A

Inflammation of the vestibular nerve (after a viral infection)
Secondary to ischaemia of the anterior vestibular artery

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151
Q

How to differentiate vestibular neuronitis with labyrinthitis

A

hearing is not affected in vestibular neuronitis.

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152
Q

List the complications in vestibular neuronitis

A

BPPV
Persistent postural perceptual dizziness (PPPD)
Oscilloposia

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153
Q

List the presentations in vestibular neuronitis

A

Spontaneous vertigo
* Exacerbated by changes of head position
* Acute symptoms settle in a few days and recovery over 2–6 weeks.
Imbalance (veer to the affected side)
Nausea and vomiting
Autonomic symptoms
* Malaise
* Pallor
* Sweating

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154
Q

Give the ocular sign in vestibular neuronitis

A

Nystagmus with the fast phase away from the affected ear

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155
Q

Give the symptomatic managements for nausea, vomiting, vertigo in vestibular neuronitis

A

Buccal prochlorperazine
Intramuscular prochlorperazine / cyclizine

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156
Q

List the four characteristic features of Parkinsonism

A

Bradykinesia
Tremor
Rigidity
Postural instability

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157
Q

List the causes of Parkinsonism

A

Parkinson’s disease
Vascular Parkinsonism
Drug induced
Parkinson-plus syndromes
* Lewy body dementia
* Multiple system atrophy
* Progressive supranuclear palsy
* Corticobasal degeneration
Wilson’s disease
Repeated head injury

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158
Q

List the drugs that may cause Parkinsonism

A

First generation antipsychotics (fluphenazine, trifluoperazine, haloperidol, chlorpromazine, flupentixol, zuclopenthixol)
Antiemetics (prochlorperazine, metoclopramide)

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159
Q

List the symptoms in multiple system atrophy

A

Parkinsonism
Severe early autonomic dysfunction:
* Symptomatic hypotension
* Constipation / Urinary retention
* Faecal / Urinary urge incontinence
* Persistent erectile dysfunction
Speech/bulbar dysfunction
Pyramidal/cerebellar dysfunction
Poor response to levodopa

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160
Q

List the symptoms of progressive supranuclear palsy

A

Parkinsonism
Early dysphagia
Vertical gaze palsy
Recurrent falls (postural instability)

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161
Q

List the symptoms of corticobasal degeneration

A

Parkinsonism
Asymmetric rigidity and dystonia
Cortical sensory loss
Progressive aphasia
Apraxia
Cognitive impairment
Alien limb phenomenon

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162
Q

List the symptoms of Wilson’s disease

A

Kayser-Fleischer rings
Variable neurological signs including tremor, ataxia, dystonia
Non-specific liver disease

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163
Q

List the symptoms in Parkinson’s disease

A

Tremor at rest
Rigidity
Bradykinesia
Postural instability
Autonomic dysfunction
* Orthostatic hypotension
* Swallowing problems
* Excessive salivation
* Weight loss
* Urinary symptoms
* Constipation
* Sexual problems
Non-motor symptoms
* Depression, anxiety, and fatigue
* Anosmia
* Cognitive impairment
* REM sleep behaviour disorder
* Pain

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164
Q

List the pathologies in Parkinson’s disease

A

Selective loss of nigrostriatal dopaminergic neurons in the substantia nigra pars compacta (SNc)
Intracytoplasmic eosinophilic inclusions (Lewy bodies) and neurites, composed of alpha-synuclein

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165
Q

Give the pathophysiology in Parkinson’s disease

A
  1. Decreased activity of the direct pathway and increased activity of the indirect pathway
  2. Increased inhibitory activity from the GPi/SNr to the thalamus
  3. Reduced output to the cortex
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166
Q

List the symptomatic management options in Parkinson’s

A

Levodopa
Monoamine oxidase-B (MAO-B) inhibitors
* Selegiline
* Rasagiline
* Safinamide
Dopamine agonists
* Pramipexole (oral)
* Ropinirole (oral)
* Rotigotine (transdermal)

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167
Q

List the side effects of levodopa

A

Dyskinesia
Excessive sleepiness
Hallucinations
Impulse control disorders

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168
Q

List the causes of tremor

A

Essential tremor
Postural and action tremor
* Dystonic tremor
* Hyperthyroidism
* Drugs eg. beta2-agonists
Intention tremor - cerebellar disorder

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169
Q

List the presentations in essential tremor

A

Postural tremor - worse if arms outstretched
Bilateral and symmetrical
Involves the head, neck, voice, and limbs
Worsen with
* stress
* caffeine
* sleep deprivation
Improves
* alcohol
* beta-blockers

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170
Q

List the presentations in Huntington’s disease

A

Chorea
Incoordination
Cognitive decline
Personality changes
Psychiatric symptoms

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171
Q

List the causes of chorea

A

Systemic disease
* Thyrotoxicosis
* SLE
* Antiphospholipid syndrome
* Polycythaemia vera
Genetics
* Huntington’s disease
* Neuroacanthocytosis
* Benign hereditary chorea
Structural and vascular disorders of the basal ganglia
Drugs
* Levodopa
* Oral contraceptives
Post-infectious (Sydenham’s chorea)
Pregnancy

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172
Q

List the management options for depression in Huntington’s disease

A

Fluoxetine (SSRI)
Buspirone
Benzodiazepines

173
Q

Give the inheritance and genetic mechanism in myoclonic dystonia

A

Autosomal dominant disorder
Mutation in ε-sarcoglycan gene

174
Q

List the characteristics in Tourette’s syndrome

A

Childhood onset
Motor and vocal tics
Psychiatric disorders (OCD, ADHD)

175
Q

Give the first line management for tics in Tourette’s syndrome

A

Comprehensive behavioural intervention for tics

176
Q

List the pharmacological therapies in Tourette’s syndrome

A

Alpha-2 agonist (monotherapy at minimal dosage)
* Clonidine
* Guanfacine
Antipsychotics
* Aripiprazole
* Risperidone
* Ziprasidone
Botulinum toxin

177
Q

Define geste antagoniste

A

Dystonia may improve with simple ‘sensory tricks’ such as lightly touching the affected body part

178
Q

List the presentations in focal dystonia

A

Axial
* Blepharospasm
* Cervical torticollis
Limb
* Task related (writer’s cramp)
* Foot
* Orofacial/mandibular

179
Q

Give one cause of early-onset (<26 years) dystonia

A

TOR1A gene mutations

180
Q

List the management options of generalised dystonias

A

Levodopa
Trihexyphenidyl (anticholinergic)
Pallidal deep brain stimulation

181
Q

List the four clinical patterns of motor neurone disease

A

Amyotrophic lateral sclerosis
Progressive muscular atrophy
Progressive bulbar and pseudobulbar palsy
Primary lateral sclerosis

182
Q

List the presentations in progressive muscular atrophy

A

Pure LMN presentation
Weakness
Muscle wasting
Fasciculations
Usually starting in one limb and gradually spreading to involve other adjacent spinal segments

183
Q

List the presentations of primary lateral sclerosis

A

UMN disorder
Slowly progressive tetraparesis and pseudobulbar palsy

184
Q

List the UMN signs

A

Mild weakness
Spasticity
Hyperreflexia and clonus
Pathological reflexes:
* Babinski
* Hoffmann sign
* Loss of abdominal reflexes

185
Q

List the LMN signs

A

Moderate to severe weakness
Atrophy
Hyporeflexia
Flaccidity
Fasciculations

186
Q

List the aetiologies in ALS

A

Sporadic (mostly)
Genetic
* free radical scavenging enzyme superoxide dismutase (SOD-1) - missense mutations
* C9orf72
* TDP-43
* FUS

187
Q

List the initial symptoms in ALS

A

Isolated dysarthria
Hand weakness
Foot drop
Gait changes
Shortness of breath

188
Q

What is familial ALS associated with

A

FTD

189
Q

List the physical examination findings in ALS

A

Typical UMN findings:
Loss of coordinated movement
Spasticity
Muscle spasms
Pronator drift
Hyperreflexia
* Babinski’s sign
* Hoffmann’s reflex
* Crossed adductors
* Exaggerated jaw jerk
* Primitive reflexes: palmomental/snout reflex

Typical LMN findings:
Weakness
Atrophy
Fasciculations

Split-hand phenomenon - severe changes in the thenar eminence but relative sparing of the hypothenar eminence

190
Q

Give the diagnostic criteria in ALS

A

(El Escorial Diagnostic Criteria)

Definite ALS - UMN and LMN signs in at least 3 regions
Probable ALS - UMN and LMN signs in 2 regions, with some UMN signs rostral to LMN signs

191
Q

List the investigations for ALS

A

Nerve conduction studies
* Diminished CMAP
* Normal sensory nerve conduction study
Electromyography
* Fasciculation potentials
* Acute (positive sharp waves and fibrillation potentials) + chronic (reduced neurogenic firing pattern, polyphasic motor unit potentials) changes

192
Q

List other tests to exclude in ALS

A

Nerve conduction studies - Rule out peripheral nerve disease mimicking ALS eg. multifocal motor neuropathy
If NCS suggests possible peripheral nerve disease, blood tests to assess:
* Vitamin B₁₂ level
* Specific antibodies (anti-GM1, acetylcholine receptor, muscle-specific tyrosine kinase, voltage-gated calcium-channel antibodies)
Neuroimaging - Exclude structural, inflammatory, or infiltrative disorders
Lumbar puncture - Exclude infectious diseases

193
Q

Give the 1st line and alternative Disease-modifying pharmacological therapies for ALS

A

1st line: Riluzole
Edaravone (antioxidant)
Sodium phenylbutyrate / tauroursodeoxycholic acid

194
Q

Give the mechanism of Riluzole

A

Glutamate inhibitor, reduces excitotoxicity

195
Q

Give two adverse effects associated with riluzole

A

Hepatotoxicity and neutropenia (rare)
LFT and FBC monthly for first 3 months, then every 3 months

196
Q

Give the mutation in DMD and Becker muscular dystrophy

A

Dystrophin - exon deletions

197
Q

Give the inheritance of DMD

A

X-linked recessive

198
Q

What do the mutations in Emery-Dreifuss muscular dystrophy affect

A

Nuclear envelope proteins
* Emerin (X-linked recessive)
* Lamin A/C (autosomal dominant)

199
Q

Give the mutations in Facioscapulohumeral muscular dystrophy

A

Small deletion on chromosome 4 affecting
D4Z4 region in FSHD1 (95%)
SMCHD1 region in FSHD2

200
Q

Give the inheritance in Facioscapulohumeral muscular dystrophy

A

Autosomal dominant
Spontaneous mutations (up to 30%)

201
Q

Give the mutation in Myotonic dystrophy type 1 (DM1)

A

CTG triplet repeat expansion in the 3’ non-coding region of DMPK

202
Q

Give the onset age for Limb-girdle muscular dystrophies

A

10~20 years

203
Q

Give the onset age for Facioscapulohumeral muscular dystrophy

A

10–40 years

204
Q

What muscles are predominantly affected in Limb-girdle muscular dystrophies

A

Proximal: shoulders, pelvic girdle

205
Q

What muscles are predominantly affected in facioscapulohumeral muscular dystrophies

A

Face, shoulders, scapular winging, upper arms, foot drop.
Typically asymmetric

206
Q

What are the associated features in facioscapulohumeral muscular dystrophies

A

deafness and retinal abnormalities

207
Q

Give the prognosis in Limb-girdle muscular dystrophies

A

Severe disability <25 years

208
Q

Give the prognosis in facioscapulohumeral muscular dystrophies

A

Life expectancy normal, slow progression

209
Q

Give the pathophysiology in DMD

A

Xp21 defect / deletion results in the absence of dystrophin (sarcolemma-associated protein)
Provides structural stability to the dystroglycan complex in cell membranes
Results in ongoing cell membrane depolarisation due to calcium entering the cell
Causes ongoing degeneration and regeneration of muscle fibres
Degeneration is faster than regeneration, and muscle fibres undergo necrosis
Muscle fibres are replaced by adipose and connective tissue, causing the muscles to progressively weaken

210
Q

List the classic presentation in Duchenne muscular dystrophy

A

Toddler with
* Delayed motor milestones
* Calf hypertrophy
* Proximal hip girdle muscle weakness
* Marked elevation of serum creatine kinase

211
Q

List the physical examination findings in Duchenne muscular dystrophy

A

Imbalance of strength at all lower extremity pivots
Relatively weaker hip extensors, knee extensors, and ankle dorsiflexors
Physical signs:
* Gowers’ sign
* Musculotendinous contractures - imbalance of lower body strength
* Increased lumbar lordosis and heel cord contractures

212
Q

List the management options for DMD

A

Corticosteroid therapy - Preserve muscle strength
Prevention/reduction of musculotendinous contractures
Physiotherapy

213
Q

List the novel oral direct factor Xa inhibitors

A

Apixaban
Betrixaban
Edoxaban
Rivaroxaban

214
Q

List the novel oral direct factor IIa inhibitors

A

Dabigatran

215
Q

List the presentations in Anterior cerebral artery syndrome

A

Contralateral hemiparesis and sensory loss of lower limbs
Anosmia
Anterior corpus callosum involvement - alien hand syndrome
Pericallosal branch involvement - apraxia, agraphia, tactile anomia of the left hand

216
Q

List the presentations in infarction of the Inferior division of dominant MCA

A

Contralateral homonymous hemianopia or upper quadrant anopsia
Receptive aphasia (Wernicke)

217
Q

List the presentations in infarction of the superior division of dominant MCA

A

Contralateral weakness (affects the lower face and arm more than the leg)
Contralateral sensory loss (including the face)
Contralateral hemineglect
Expressive aphasia (Broca)

218
Q

List the presentations in infarction of the Whole of the dominant MCA

A

(Gerstmann syndrome)
Agraphia, Acalculia, Finger agnosia
Right-left disorientation
Contralateral weakness, sensory loss
Contralateral hemineglect
Contralateral homonymous hemianopia
Global aphasia (receptive and expressive)

219
Q

List the signs of elevated ICP

A

Reducing level of consciousness
Severe headache
Nausea/vomiting
Sudden increase in blood pressure

220
Q

Give the presentations in occlusion of one of the paramedian branches of the basilar artery

A

Weber syndrome (Ventromedial midbrain)
* Ipsilateral oculomotor nerve palsy
* Contralateral hemiplegia

221
Q

Give the presentations in Anterior inferior cerebellar artery (AICA) infarction

A

(Lateral pontine syndrome (Marie-Foix Syndrome))
Ipsilateral cerebellar ataxia (arm and leg)
Ipsilateral facial weakness
Ipsilateral deafness, vertigo, nystagmus (CN VIII palsy)
Contralateral weakness (corticospinal tract)
Contralateral pain and temperature loss (spinothalamic tract)

222
Q

List the presentations in Posterior inferior cerebellar artery (PICA) infarction

A

(Lateral medullary syndrome (Wallenberg Syndrome))
Ipsilateral
* Loss of gag reflex
* Facial sensory loss
* Horner’s syndrome
* Nystagmus
* Ataxia
Contralateral - Pain and temperature sensory loss in the extremities
Generally
* Vertigo
* Nausea
* Dysphagia

223
Q

Give the transitional therapy options in cluster headache

A

Prednisolone
IV dihydroergotamine (Contraindicated in patients with CV risk factors (CAD, HTN))
Greater occipital nerve block

224
Q

List the severity grading and mortality in TBI

A

Mild TBI: GCS 13-15; mortality 0.1%
Moderate TBI: GCS 9-12; mortality 10%
Severe TBI: GCS <9; mortality 40%

225
Q

List the aetiologies for TBI

A

Blunt TBI
* Falls (48%)
* Motor vehicle-related injury (17%)
* Crush injuries
* Physical altercations
Penetrating TBI
* Gunshot
* Stabbing
Blast TBI - combination of contact and inertial forces, overpressure, and acoustic waves

226
Q

What is Diffuse axonal injury

A

Rapid rotational/deceleration force that causes stretching and tearing of neurons, followed by focal areas of haemorrhage and oedema.

227
Q

List the CT grading for Diffuse axonal injury

A

Petechial haemorrhages and oedema located at the:
Grey-white matter junction (Grade 1)
Corpus callosum (Grade 2)
Brainstem (Grade 3)

228
Q

List the primary interventions to elevated intracranial pressure

A

Raising the head of the bed to 30°
Analgesics and sedation - reduce metabolic demands
Inducing hypocapnia by hyperventilation - reduces pCO₂, which provokes cerebral vasoconstriction, and lowers ICP
* Hyperventilation should be limited to <30 minutes to treat acute cerebral herniation.

229
Q

List the secondary interventions to elevated intracranial pressure

A

Osmosis: hypertonic saline, mannitol
High-dose barbiturate
ICP monitoring
Decompressive hemicraniectomy

230
Q

List the six cognitive domains

A

attention
executive function
memory and learning
language
perceptual motor
social cognition

231
Q

Give the DSM5 diagnostic criteria for Major Neurocognitive Disorder/Dementia

A

Significant cognitive decline in one or more cognitive domains, based on:
1. Concern about significant decline, expressed by individual/reliable informant/observed by clinician.
2. Substantial impairment, documented by objective cognitive assessment.
Interference with independence in everyday activities.
Not exclusively during delirium.
Not better explained by another mental disorder.
Specify one or more etiologic subtypes

232
Q

Define Idiopathic intracranial hypertension

A

Increased intracranial pressure in an alert and oriented patient

233
Q

In what population does Idiopathic intracranial hypertension predominantly occur?

A

overweight women of childbearing years, often in the setting of weight gain.

234
Q

Give the pathophysiology in Idiopathic intracranial hypertension

A

CSF absorption occurs both via the arachnoid granulations and along nerve root sheaths, especially along the olfactory nerve through the cribriform plate.
Abnormalities of the absorption pathways.
Papilloedema and loss of vision are usually due to intraneuronal ischaemia related to increased CSF pressure transmitted along the optic nerve sheath.

235
Q

List the symptoms and signs of Idiopathic intracranial hypertension

A

Symptoms
* Headaches
* Pulse-synchronous tinnitus
* Transient visual obscurations, visual loss, diplopia
* Neck and back pain
Signs
* Papilloedema
* CN6 paresis
* Sensory visual disturbances

236
Q

List the secondary causes of intracranial hypertension

A

Decreased flow through arachnoid granulations due to scarring from previous inflammation
* Meningitis
* Sequel to subarachnoid haemorrhage
Obstruction to venous drainage
* Venous sinus thrombosis
* Bilateral radical neck dissection
* Superior vena cava syndrome
* Increased right heart pressure
Endocrine disorders
* Addison’s disease
* Hypoparathyroidism
* Corticosteroid withdrawal
Hypervitaminosis A (vitamin, liver, or isotretinoin intake)
Arteriovenous malformations and dural shunts

237
Q

List the investigations and findings in Idiopathic intracranial hypertension

A

Lumbar puncture - opening pressure >250 mm H2O
MRI
* Transverse sinus stenosis
* Empty sella
* Posterior globe flattening
* Pituitary stalk displacement
* Meningoceles
* Abnormalities of the optic nerve
* Slit like ventricles
* Tight subarachnoid spaces
Inferior position of cerebellar tonsils

238
Q

List the non-medical management options for Idiopathic intracranial hypertension

A

Weight-reduction
Low-sodium diet

239
Q

List the medical management options for Idiopathic intracranial hypertension

A

Acetazolamide
Furosemide
Topiramate

240
Q

List the mechanisms of Acetazolamide in treating Idiopathic intracranial hypertension

A

Inhibit carbonic anhydrase, reduces sodium ion transport across the choroid plexus epithelium
Acetazolamide decreases CSF production in humans by 6~50%

241
Q

List the contents in cavernous sinus

A

CN III, IV, V1, V2, VI
Internal carotid artery

242
Q

List the sources of cavernous sinus

A

Superior and Inferior ophthalmic vein
Superficial middle cerebral vein
Middle meningeal vein
Hypophyseal veins

243
Q

Where does cavernous sinus drain to

A

Superior and inferior petrosal sinuses

244
Q

List the septic causes of Cavernous sinus thrombosis

A

Sinusitis
Facial infection (folliculitis)
Periorbital infection.
Mucormycosis (highly invasive fungal infection, usually occurs in immunocompromised)
Otitis media, mastoiditis
Petrous apicitis (infection of the medial portion of the temporal bone at the base of the skull)
Odontogenic infection
Bacterial meningitis

245
Q

List the aseptic causes of Cavernous sinus thrombosis

A

Trauma
Post-surgery
Hypercoagulable states
Malignancy
* Rhabdomyosarcoma
* Nasopharyngeal carcinoma
Vascular abnormalities

246
Q

List the Hypercoagulable states

A

Polycythaemia vera
Sickle cell disease
Acute lymphocytic leukaemia
Deficiencies of antithrombin III, protein C, or protein S
Resistance to activated protein C
Antiphospholipid syndrome
Thrombocytosis
Elevated IgM
Nephrotic syndrome
Oral contraceptives

247
Q

What is the most common causative organism for septic Cavernous sinus thrombosis

A

Staphylococcus aureus

248
Q

List the causative organisms in septic Cavernous sinus thrombosis

A

Staphylococcus aureus (most common)
Fusobacterium necrophorum
Streptococci

249
Q

List the presentations in Cavernous sinus thrombosis

A

Headache - unilateral, V1/2 regions (retro-orbital or frontal areas)
Fever (septic CST)
Ocular manifestations
* Chemosis (conjunctival oedema)
* Periorbital oedema
* Proptosis.​
* Painful ophthalmoplegia
* Ptosis
* Mydriasis
* External ophthalmoplegia (restriction of extraocular muscles)

250
Q

Give the investigation and finding in Cavernous sinus thrombosis

A

CT with contrast - abnormal filling defects with lateral convexity of the cavernous sinuses

251
Q

List the managements in Cavernous sinus thrombosis

A

Empirical antibiotics: vancomycin with/without rifampicin
Linezolid
Trimethoprim/sulfamethoxazole

252
Q

Give the level of motor lesion in bulbar palsy and pseudobulbar palsy

A

Bulbar - LMN
Pseudobulbar - UMN

253
Q

List the clinical features in bulbar palsy

A

Tongue - wasted, fasciculations
Absent palatal movement
Absent gag reflex
Absent jaw jerk
Nasal speech (flaccid dysarthria)
Normal emotions

254
Q

List the causes of bulbar palsy

A

Motor neurone disease
Syringobulbia
Guillain-Barre syndrome
Poliomyelitis
Subacute menignitis (carcinoma, lymphoma)
Neurosyphilis
Brainstem cerebrovascular accident

255
Q

What is the most common cause for pseudobulbar palsy

A

Bilateral cerebrovascular accidents affecting the internal capsule

256
Q

List the causes for pseudobulbar palsy

A

Cerebrovascular accidents
Multiple sclerosis
Motor neurone disease
High brainstem tumours
Head injury

257
Q

List the clinical features in pseudobulbar palsy

A

Spastic tongue, slow moving
Absent palatal movement
Increased gag reflex
Increased jaw jerk
Spastic speech, ‘Donald Duck’ dysarthria
Labile emotions

258
Q

Describe the gait in Parkinson’s disease and other Parkinsonian syndromes

A

Stooped posture
Shuffling (reduced stride length)
Loss of arm swing
Postural instability
Freezing

259
Q

Describe the gait in muscular dystrophies and acquired myopathies

A

(Myopathic gait)
Waddling (proximal weakness)
Bilateral Trendelenburg signs

260
Q

Describe the gait in common peroneal nerve palsy

A

Foot drop

261
Q

Describe the gait in cerebellar disease

A

(Central ataxia)
Wide-based, ‘drunken’
Tandem gait poor

262
Q

Describe the gait in sensory ataxia

A

Wide-based
Positive Romberg sign

263
Q

List the causes of positive Romberg sign

A

Sensory ataxia
Bilateral vestibular failure

264
Q

Describe the gait in Hemiplegia

A

The foot on the affected side is plantar flexed and describes a semicircle as the patient walks
The upper limb may be flexed

265
Q

Describe the gait in bilateral UMN damage

A

Scissor-like gait (spasticity)

266
Q

List the drugs commonly causing tremor

A

Sodium valproate
Glucocorticoids
Lithium

267
Q

Describe the tremor in Parkinson’s disease

A

slow (3 to 7 Hz), coarse, ‘pill-rolling’ tremor, worse at rest but reduced with voluntary movement

268
Q

Describe Physiological tremor

A

fine (low-amplitude), fast (high-frequency, 3 to 30 Hz) postural tremor

269
Q

List the Medical Research Council grading of muscle power

A

0 - No muscle contraction visible
1 - Flicker of contraction but no movement
2 - Joint movement when effect of gravity eliminated
3 - Movement against gravity but not against resistance
4 - Movement against resistance but weaker than normal
5 - Normal power

270
Q

List the nerve and muscle supplies of shoulder abduction

A

Deltoid - Axillary C5

271
Q

List the nerve and muscle supplies of:
Elbow flexion
Elbow extension

A

Elbow flexion
* Biceps - Musculocutaneous C5/6
* Brachioradialis (supinator reflex) - Radial C6
Elbow extension
* Triceps - Radial C7

272
Q

List the nerve and muscle supplies of:
Wrist extension

A

Extensor carpi radialis longus - Radial (posterior interosseous branch) C6

273
Q

List the nerve and muscle supplies of:
Finger extension
Finger flexion

A

Finger extension
* Extensor digitorum communis - Radial (posterior interosseous branch) C7
Finger flexion
* Flexor pollicis longus/Flexor digitorum profundus - Median (anterior interosseous branch) C8
* Flexor digitorum profundus - Ulnar C8

274
Q

List the nerve and muscle supplies of:
Finger abduction
Thumb abduction

A

Finger abduction
* First dorsal interosseous - Ulnar T1
Thumb abduction
* Abductor pollicis brevis - Median T1

275
Q

List the nerve and muscle supplies of:
Hip flexion
Hip extension

A

Hip flexion
* Iliopsoas - Iliofemoral nerve L1/2
Hip extension
* Gluteus maximus - Sciatic L5/S1

276
Q

List the nerve and muscle supplies of:
Knee flexion
Knee extension

A

Knee flexion
* Hamstrings - Sciatic S1
Knee extension
* Quadriceps - Femoral L3/4

277
Q

List the nerve and muscle supplies of:
Ankle dorsiflexion
Ankle plantar flexion

A

Ankle dorsiflexion
* Tibialis anterior - Common peroneal L4/5
Ankle plantar flexion
* Gastrocnemius and soleus - Tibial S1/2

278
Q

List the nerve and muscle supplies of:
Great toe extension (dorsiflexion)

A

Extensor hallucis longus - Common peroneal L5

279
Q

List the nerve and muscle supplies of:
Ankle eversion
Ankle inversion

A

Ankle eversion
* Peronei - Common peroneal L5/S1
Ankle inversion
* Tibialis posterior - Tibial nerve L4/5

280
Q

What may isolated loss of a reflex suggest

A

mononeuropathy
radiculopathy

281
Q

What may unilateral grasp and palmomental reflexes suggest

A

Contralateral frontal lobe pathology

281
Q

List the causes of Bell’s palsy

A

Ramsay Hunt syndrome (herpes zoster infection of the geniculate (facial) ganglion)
Vestibular schwannoma (cerebellopontine angle compression)
Parotid tumours
Trauma

282
Q

List the features in Bell’s palsy

A

(LMN CN7 paralysis)
Weakness of both upper and lower facial muscles
Taste impairment
Hyperacusis

283
Q

What is anterior cord syndrome caused by

A

Anterior vertebral artery injury eg. flexion injury

284
Q

What is the most common cause of central recurrent attacks of vertigo

A

Migraine

285
Q

Give the pathophysiology in cervical spondylotic radiculopathy

A

Mechanical compression/chemical irritation of a specific nerve root by
* degenerative disc
* degenerative joint changes, narrowing the root exit at the foraminal level

286
Q

Give the pathophysiology in degenerative cervical myelopathy

A

Posterior disc protrusion
Congenital spinal canal narrowing
Osteophytic bars
Ligamentous thickening
Ischaemia

287
Q

Give the managements in malignant spinal cord compression

A

Corticosteroid - dexamethasone sodium phosphate
Radiotherapy
Surgery

288
Q

Give the landmark for conus medullaris

A

T12-L1

289
Q

Contrast the presentations in cauda equina syndrome vs conus medullaris syndrome

A

CES (LMN involvement)
* Usually bilateral, severe radicular pain
* Saddle anaesthesia
* Asymmetric motor weakness
* Hypo/areflexia
* Late-onset bowel/bladder dysfunction

CMS (Mixed UMN and LMN involvement)
* Sudden-onset severe back pain
* Perianal anaesthesia
* Symmetric motor weakness
* Hyperreflexia
* Early-onset bowel/bladder dysfunction

290
Q

List the clinical presentations in cauda equina syndrome

A

Low back pain
Bilateral / unilateral sciatica
Saddle anaesthesia / paraesthesia
Sexual dysfunction
Bladder dysfunction
* Difficulty starting/stopping urination
* Impaired sensation of urinary flow
* Urgency
* Urinary retention with overflow urinary incontinence
Bowel dysfunction
* Loss of sensation of rectal fullness
* Faecal incontinence
* Laxity of the anal sphincter

291
Q

Give the investigation for cauda equina syndrome

A

MRI lumbar spine without IV contrast

292
Q

What diseases may affect the anterior horn cells?

A

Anterior poliomyelitis
Motor neuron disease

293
Q

What may axonal degeneration be caused by

A

Systemic metabolic disorders
Toxin exposure
Vasculitis
Inherited neuropathies

294
Q

What does axonal degeneration present as

A

Stocking and glove sensory loss
Muscle weakness and atrophy
Loss of distal limb myotatic reflexes

295
Q

Give the presentation when anterior horn cells are affected

A

Focal weakness without sensory loss

296
Q

Give the presentation when dorsal root ganglion neurons are affected

A

Sensory ataxia
Sensory loss
Diffuse areflexia

297
Q

What diseases may affect the dorsal root ganglion neuron?

A

Toxins
* organic mercury compounds
* doxorubicin
* high-dose pyridoxine
Vitamin E deficiency
Immune-mediated
* paraneoplastic sensory neuronopathy
* Sjögren syndrome

298
Q

List the types of nerve fibres

A

Sensory - large myelinated
Motor - small myelinated
Autonomic - small unmyelinated

299
Q

List the presentations in L5 Radiculopathy

A

Foot drop
Weak ankle inversion

300
Q

List the presentations in Sciatic nerve L4~S3 palsy

A

Paralysis of knee flexion and all movements below knee
Sensory loss below knee
Reflexes
* ankle and plantar reflex lost
* knee jerk intact

301
Q

List the presentations in Tibial nerve L4~S3 palsy

A

Inability to
* Stand on tiptoe (plantar flexion)
* Invert the foot
* Flex the toe
* Sensory loss over the sole

302
Q

Give the Median nerve root

A

C6-T1

303
Q

What other conditions may be carpal tunnel syndrome be seen in

A

Hypothyroidism
Pregnancy (third trimester)
Rheumatoid disease
Acromegaly
Amyloidosis, including dialysis

304
Q

List the risk factors for carpal tunnel syndrome

A

variations in the anatomy of the carpal tunnel
age over 30 years
high BMI
pregnancy
occupations involving repetitive movements of the wrist

305
Q

List the clinical presentations for carpal tunnel syndrome

A

Gradual onset, intermittent, bilateral hand numbness and pain
Numbness typically confined to the palmar aspect of the thumb and radial fingers
Sensory loss in the radial 3.5 fingers.
Thenar muscle wasting
Waking up at night-time
Difficulty finger extension / flexion on awakening
Relived by shaking or flicking the wrist

306
Q

Give the gold standard investigation in carpal tunnel syndrome and findings

A

Electromyography
* conduction velocity slowing in the median sensory nerves across the carpal tunnel
* median distal motor latency prolongation
* decreased amplitude of median sensory/motor nerves

307
Q

Give the ulnar nerve root and list the ulnar neuropathy presentation

A

Ulnar nerve root = C8-T1

Claw hand
Wasting of interossei and hypothenar muscles
Weakness of interossei and medial two lumbricals
Sensory loss in the little finger and splitting of the ring finger

308
Q

Give the radial nerve root and list the radial neuropathy presentation

A

Radial nerve root = C5-T1

Wrist drop
Weakness of brachioradialis and finger extension

309
Q

What is meralgia paraesthetica caused by? Give its presentation

A

Compression of the lateral femoral cutaneous nerve (L2-3)
Anterio-lateral burning thigh pain

310
Q

Give the common peroneal nerve root and list the common peroneal neuropathy presentation

A

Common peroneal nerve root = L4-S2

Foot drop
Intact ankle jerk (S1)
Weakness of
* ankle eversion
* foot dorsiflexion
Sensory loss over the dorsum of the foot and the lower lateral part of the leg
Wasting of the anterior tibial and peroneal muscles

311
Q

Name two branches of the sciatic nerve

A

Divides into tibial and common peroneal nerves

312
Q

In what conditions may mononeuritis multiplex occur in

A

Vasculitis
Diabetes mellitus
Malignancy
Neurofibromatosis
HIV and hepatitis C infection
Leprosy
Multifocal motor neuropathy with conduction block.

313
Q

Give the presentation in mononeuritis multiplex

A

Painful, acute to subacute sensory and motor deficits that may be limited to one nerve or multifocal.

314
Q

Give the typical presentations in polyneuropathies

A

Symmetric numbness, paraesthesias, and dysesthesias in the feet and distal lower extremities.
Stocking-glove sensory symptoms in severe cases

315
Q

List the specific etiologies for demyelinating polyneuropathy

A

Guillain–Barré syndrome
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)
Monoclonal gammopathies
Hereditary neuropathies

316
Q

List the neuropathies with Autonomic Nervous System Involvement

A

Acute
* Acute pandysautonomic neuropathy (autoimmune, paraneoplastic)
* Guillain-Barré syndrome
* Porphyria
* Toxic: vincristine
Chronic
* Diabetes mellitus
* Amyloid neuropathy
* Paraneoplastic sensory neuronopathy (malignant inflammatory sensory polyganglionopathy)
* HIV-related autonomic neuropathy
* Hereditary sensory and autonomic neuropathy

317
Q

Give the aetiology for Guillain–Barré syndrome

A

Infections in the 6 weeks before symptom onset
Campylobacter jejuni
Cytomegalovirus
Epstein–Barr virus
Mycoplasma pneumoniae

318
Q

List the symptoms and signs in Guillain–Barré syndrome

A

Paraesthesias in hands and feet
Pain (typically begins in the back and legs)
Hyporeflexia/areflexia
Facial, oropharyngeal, and extraocular weakness (cranial nerve deficits)
Dysautonomia
* Sinus tachycardia, Cardiac arrhythmias
* Hypertension, postural hypotension
* Urinary retention, Ileus
Respiratory muscle weakness
* Dyspnoea on exertion
* Shortness of breath

319
Q

List the investigations and findings in Guillain–Barré syndrome

A

Lumbar puncture - Increased CSF albumin with a normal cell count (albuminocytological dissociation)
Nerve conduction studies
* Prolonged distal and F-wave latencies
* Reduced conduction velocities
LFT - Elevated AST, ALT
Spirometry - reduced:
* Vital capacity
* Maximal inspiratory/expiratory pressure

320
Q

List the management options for Guillain–Barré syndrome

A

high-dose intravenous immunoglobulin (IVIG)
plasma exchange

321
Q

List the causes for Wernicke–Korsakoff’s syndrome

A

(Thiamine (vitamin B1) deficiency)
Alcohol (most common)
Anorexia nervosa
Vomiting of pregnancy

321
Q

List the physical examination findings in Charcot-Marie-Tooth disease

A

Sensory ataxia
Reduced strength in the distal muscles with associated atrophy and weakened foot eversion
Reduction in pinprick and vibration sensation, more pronounced distally than proximally
Areflexia/hyporeflexia
High-arched feet and hammer toes (pes cavus)
Steppage gait

321
Q

List the presentations in Wernicke–Korsakoff’s syndrome

A

Eye signs
* Nystagmus
* Bilateral lateral rectus palsies
* Conjugate gaze palsies
Ataxia
* Broad-gait based gait
* Cerebellar signs
* Vestibular paralysis
Cognitive change
* Stupor and coma (acute)
* Amnestic syndrome with confabulation (chronic)

321
Q

List the key features in Charcot-Marie-Tooth disease

A

Clumsiness as a child
Weak ankles
Steppage gait
Pes cavus (high foot arches with hammer toes)
Distal atrophy of the hands and legs (inverted champagne bottle legs)
Abnormal sensations typically begin distally and proceed proximally over time
Kyphoscoliosis
Symmetrical nerve conduction changes

321
Q

Name the most common type of Charcot-Marie-Tooth disease, inheritance, and genetic mechanisms

A

CMT 1A - most common
Autosomal dominant
PMP22 gene duplication

321
Q

Define CMT type 1 and CMT2

A

CMT type 1 (CMT1) - demyelinating conductions and dominant inheritance
CMT2 - axonal conductions and dominant inheritance

321
Q

What does dietary deficiency of Thiamine (vitamin B1) cause

A

beriberi
* Polyneuropathy
* Cardiac failure

322
Q

Give the typical presentation in Pyridoxine (vitamin B6) deficiency

A

limb numbness developing during anti-tuberculosis therapy with slow isoniazid acetylators

323
Q

How is Pyridoxine (vitamin B6) deficiency prevented

A

Prophylactic pyridoxine 10 mg daily is given with isoniazid

324
Q

List the presentations of Vitamin B12 (cobalamin) deficiency

A

Subacute combined degeneration of the cord (SACD)
* spastic paraparesis
* loss of vibration sense, proprioception, and two-point discrimination
* ataxic gait
* reduced sensation

325
Q

Give the pathologies in multiple sclerosis

A

Plaques of demyelination 2~10mm in size, commonly in
* Optic nerves
* Periventricular region
* Corpus callosum
* Brainstem and cerebellar connections
* Cervical cord (corticospinal tracts and posterior columns)

326
Q

List the four main clinical patterns of MS

A

Relapsing-remitting MS
* Onset over days and typically recovery (partial/complete) over weeks.
* Average one relapse per year.
* May accumulate disability over time if they do not recover fully after relapses.
Secondary progressive MS
* Late stage MS
* Gradually worsening disability progressing slowly over years
* ~75% of patients with relapsing–remitting MS will eventually evolve into a secondary progressive phase by 35 years after onset.
Primary progressive MS
* Gradually worsening disability without relapses or remissions
* Typically presents later
* Associated with fewer inflammatory changes on MRI
Relapsing–progressive MS
* Similar to PPMS but with occasional supra-added relapses on a background of progressive disability from the outset.

327
Q

List the common presenting symptoms in multiple sclerosis

A

Optic neuritis
* Partial / total unilateral visual loss
* Pain behind the eye
* Loss of colour discrimination (particularly reds)
* Relative afferent pupillary defect - paradoxical dilation of the pupil when light is rapidly shifted from the unaffected eye to the affected eye
Transverse myelitis
* Paresthesia
* Weakness (initial flaccid paralysis, followed by spastic paralysis with hyperreflexia)
* Tight band sensation around the trunk at the level of the inflammation
* Lhermittes’ phenomenon - Shock-like sensation radiating radiating down the spine induced by neck flexion
Cerebellar syndromes - Ataxia, Vertigo, Clumsiness, Dysmetria
Brainstem syndromes
* Ataxia
* Eye movement abnormalities- Diplopia, Oscillopsia, Nystagmus, Internuclear ophthalmoplegia
Bilateral trigeminal neuralgia
Uhthoff phenomenon: symptoms worsening with increased body temperature
Urinary frequency
Bowel dysfunction (constipation)

328
Q

List the neurological signs in multiple sclerosis

A

Internuclear ophthalmoplegia - nystagmus of the abducting eye with absent adduction of the other eye
UMN signs
* Spasticity
* Hyperreflexia
Gait
* Mild dragging of the foot
* Spasticity
* Balance problems

329
Q

Give the first line investigation and findings in multiple sclerosis

A

MRI brain (high field magnet with IV gadolinium contrast)
* Hyperintensities in the periventricular white matter
* Demyelinating lesions in the spinal cord, particularly cervical

330
Q

List the LP findings in MS

A

Oligoclonal bands
CSF IgG

331
Q

Give the management for acute MS relapse

A

Oral methylprednisolone 0.5 g for 5 days
Plasma exchange

332
Q

Give the management for Secondary progressive MS

A

1st line: Siponimod or IV methylprednisolone
2nd line: Cladribine

333
Q

Give the management for Primary progressive MS

A

Ocrelizumab

334
Q

List the antibodies for neuromyelitis optica spectrum disorders (NMOSD)

A

Anti-aquaporin 4
Anti-myelin oligodendrocyte glycoprotein

335
Q

List the NMOSD adult presentations

A

Optic neuritis
Acute myelitis
Area postrema syndrome (unexplained hiccups, nausea, or vomiting)
Acute brainstem syndrome
Symptomatic narcolepsy
Symptomatic cerebral syndrome with NMOSD-typical brain lesions

336
Q

List the typical presentations in transverse myelitis

A

Typically bilateral
Progressive paraparesis/quadriparesis
Sensory loss/paraesthesias below the lesion
Autonomic (bowel and bladder) dysfunction
Evolution of signs over several days.
Radicular or segmental pain at the level of the spinal lesion
Back pain
L’hermitte’s sign
Paroxysmal tonic spasms

337
Q

List the treatment for Transverse myelitis

A

IV methylprednisolone

338
Q

Define Progressive Multifocal Leukoencephalopathy

A

Demyelinating disease preferentially affecting the CNS
Areas commonly involved
* subcortical white matter
* periventricular areas
* cerebellar peduncles
In most cases, the optic nerve and the spinal cord are unaffected.

339
Q

List the causes for Progressive Multifocal Leukoencephalopathy

A

Reactivation of John Cunningham virus (JC virus) infecting oligodendrocytes in patients with compromised immune systems.
* AIDS
* Post solid organ/bone marrow transplant recipients
* Malignancies
* Chronic inflammatory conditions

(Progressive and fatal disease)

340
Q

List the presentations for Progressive Multifocal Leukoencephalopathy

A

New-onset neurological symptoms in a patient with immunosuppression
Cognitive impairment
Limb, gait ataxia
Hemiparesis
Hemianopia
Aphasia

341
Q

Give the CT findings in Progressive Multifocal Leukoencephalopathy

A

hypodense confluent lesions without mass effect

342
Q

List the risk factors of essential tremor

A

Ageing
Genetics
Environmental toxins
* Organochlorine pesticides
* Lead
* Mercury
* Beta-carboline alkaloids (harmane, harmaline)

343
Q

List the management options for essential tremor

A

Propranolol
Primidone
Small amounts of alcohol
Benzodiazepines - clonazepam
DBS
* ventralis intermedius nucleus (VIM) of the thalamus
* caudal zona incerta (posterior subthalamic area)
Ultrasound thalamotomy
* refractory ET ineligible for DBS

344
Q

Give the inheritance and genetic mechanism in Huntington’s disease

A

Autosomal dominant

Expanded CAG repeats at the N-terminus of the HTT gene that codes for huntingtin protein.
Individuals with ≥40 CAG repeats are certain to develop Huntingon’s disease.
Reduced penetrance is observed in those with 36 to 39 repeats.

345
Q

Give the pathology in Huntington’s disease

A

Degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia

346
Q

Define Posthypoxic myoclonus

A

A form of secondary myoclonus following cardiac arrest, divided into acute and chronic

Myoclonus status epilepticus - acute, within 24 hrs
* Generalised myoclonus
* Intermittent eye opening, upward gaze deviation, swallowing movements

Lance-Adams syndrome - chronic, days to weeks
* Focal in nature and exacerbated by action
* Negative (relaxation) myoclonus also occurs - drop objects or fall

347
Q

List the primary and secondary causes of myoclonus

A

Primary
* Physiological
* Myoclonic dystonia
* Epilepsy
Secondary
* Metabolic disorders (hepatic and renal failure, asterixis)
* Alzheimer’s
* Encephalitis

348
Q

Give the natural history in Tourette’s syndrome

A

Symptoms typically begin in childhood, peak prior to puberty, attenuate later in adolescence

349
Q

List the causes for restless legs syndrome

A

Primary - familial, autosomal dominant
Secondary
* Iron deficiency
* Pregnancy (26%, third trimester)
* Uraemia
* Renal dialysis/ESRD (20%)

350
Q

What is restless legs syndrome associated with

A

Obesity
Diabetes
Multiple sclerosis
Parkinson’s disease
Neuropathy

351
Q

What medicines can cause or worsen restless leg symptoms

A

TCAs, SSRIs
Sedating antihistamines
Metoclopramide (DPA antagonist)
Neuroleptics

352
Q

List the presentations for restless legs syndrome

A

Symptoms are nocturnal
The urge to move with dysaesthesia symptoms (creeping, crawling, tingling, cramping, aching)
Symptoms worse at rest, relieved temporarily with movement
Lower extremities are more commonly affected

353
Q

Give the McDonald diagnostic criteria for multiple sclerosis

A

(Dissemination in both time and space)
2 or more attacks + 2 or more lesions on MRI

354
Q

What population does MS classically present in

A

White women aged between 20 and 40 years.

355
Q

List the risk factors for MS

A

EBV infection
Female, caucasian, HLA-DRB1
Environmental factors
* Location (USA, europe)
* Cold climate
Low vitamin D
Smoking

356
Q

List the differential diagnoses in MS

A

Thyroid disease
Vitamin B12 deficiency
Diabetes mellitus

357
Q

List the antibodies positive in myasthenia gravis

A

Anti-AChR (80-90%)
Anti-muscle-specific tyrosine kinase (MuSK) (3-7%)

358
Q

Give the pathophysiology in myasthenia gravis

A

Circulating antibodies against the nicotinic acetylcholine receptor (AChR) or associated proteins impair neuromuscular transmission.

359
Q

List the clinical features in myasthenia gravis

A

Muscle weakness that increases with exercise (fatigue) and improves on rest.
* Ptosis, Diplopia
* Dysarthria, Dysphagia
* Facial paresis
* Proximal limb weakness
* Shortness of breath

360
Q

Define myasthenic crisis

A

An MG exacerbation requiring mechanical ventilation
* forced vital capacity ≤ 15 (normal ≥60 mL/kg)
* negative inspiratory force ≤ 20 (normal ≥70 cm H₂O)

361
Q

What may myasthenic crisis be provoked by

A

Infections (particularly respiratory infections)
Aspiration
Medicines including high-dose corticosteroids
Medications that are contraindicated in MG
Failure to adhere to medications
Administration of immune checkpoint inhibitors eg cancer therapy
Surgery
Trauma

362
Q

Give the management in myasthenic crisis

A

Intubation and mechanical ventilation
Plasma exchange / IVIG

363
Q

List the management options for myasthenic crisis

A

1st line: Pyridostigmine (cholinesterase inhibitor)
Prednisolone
Azathioprine
Rituximab (MuSK-MG)
Thymectomy

364
Q

When may thymectomy be considered in MS

A

Early in disease course for aged 18~50 to minimise the need for immunosuppressants
Ocular AChR-MG with insufficient response to cholinesterase inhibitors
Severe disease

365
Q

What conditions are associated with Lambert Eaton syndrome

A

Small cell lung cancer
Autoimmune thyroid disease
Vitamin B12 deficiency
Rheumatoid arthritis
Inflammatory myopathy
Systemic vasculitis

366
Q

What is Lambert Eaton syndrome associated with

A

Small cell lung cancer (CA-LEMS)
Autoimmune (NCA-LEMS)
* Autoimmune thyroid disease
* Vitamin B12 deficiency
* Rheumatoid arthritis
* Inflammatory myopathy
* Systemic vasculitis

367
Q

List the differences between LEMS and MG

A

MG
* Antibody against AChR Antibody
* Associated with thymic tumour
* Weakness worsen on prolonged exercise
* Normal deep tendon reflex
* Autonomic dysfunction absent
* On repeated nerve stimulation, there is decremental response

LEMS
* Antibody against voltage gated calcium channel
* Associated with small cell lung cancer
* Weakness improves on prolonged exercise
* Decreased/absent deep tendon reflex
* Autonomic dysfunction present
* On repeated nerve stimulation, there is incremental response

368
Q

Give the pathophysiology in LEMS

A

Disruption of neurotransmission due to depletion of voltage-gated calcium channels (VGCCs)
In normal neurotransmission, depolarisation of the presynaptic nerve terminal triggers calcium influx at VGCC that ultimately results in quantal release of ACh into the synaptic cleft.
This produces localised depolarisation of the adjacent peri-endplate muscle membrane.

369
Q

List the symptoms in LEMS

A

Generalised fatigue
Proximal leg weakness
Dry mouth (xerostomia), Dysarthria, Dysphagia
Prominent ocular weakness with ptosis and binocular diplopia
Autonomic features
* Pupillary dilation
* Orthostatic hypotension

370
Q

List the signs in LEMS

A

Proximal muscle weakness in hip girdle and thigh muscles
Absent/reduced tendon reflexes
Dilated, poorly reactive pupils

371
Q

List the investigations in LEMS

A

Auto-antibody serology - serum P/Q-type VGCC antibodies +ve
NCS
* Typically low initial CMAP
* Decremental responses to low-frequency repetitive nerve stimulation

372
Q

List the treatment approaches to LEMS

A

Treat malignancy
Symptomatic
* Amifampridine
* Pyridostigmine

373
Q

Give the hall mark in Prion diseases

A

Progressive dementia and motor dysfunction

374
Q

List 3 types of prion diseases

A

Sporadic Creutzfeldt-Jakob disease (sCJD)
Genetic prion diseases
* Familial CJD
* Gerstmann-Straussler-Scheinker
* Fatal familial insomnia
Acquired prion diseases
* Iatrogenic CJD
* Variant CJD

375
Q

List the investigations in prion diseases

A

MRI (FLAIR)
* hyperintensity in the cerebral cortex grey matter gyri, basal ganglia, thalamus
* bilateral pulvinar hyperintensity (vCJD)
EEG - generalised slowing, focal or diffuse, and periodic polyspike-wave complexes and sharp waves
CSF testing

376
Q

List the common metastatic brain tumours

A

Lung
Breast
Melanoma
Kidney
Stomach
Prostate
Thyroid

377
Q

List the primary malignant tumours of neuroepithelial tissue

A

Astrocytoma
Oligodendroglioma
Oligoastrocytoma
Ependymoma
Lymphoma
Medulloblastoma

377
Q

List the benign brain tumours

A

Meningioma
Neurofibroma

378
Q

List the etiological risk factors for glioma

A

Ionising radiation
Genetic syndromes
* Neurofibromatosis type 1
* Tuberous sclerosis complex
* Li-Fraumeni syndrome
* Turcot syndrome

379
Q

List the investigations and findings for meningioma

A

MRI head/spine with/without contrast
* Contrast-enhancing tumour
* Surrounding cerebral oedema
* Enhancing dural tail
CT head/spine
* Bony changes (hyperostosis)
* Calcification (25%) (slower growing tumour)
* Contrast-enhancing tumour
* Surrounding oedema, enhancing dural tail

380
Q

List the meningitis causative organisms by age group

A

Neonates
* E. coli
* Group B streptococcus (S. agalactiae)
* L. monocytogenes
Infant
* N. meningitidis
* H. influenzae
* S. pneumoniae
Young adult
* N. meningitidis
* S. pneumoniae
Elderly
* S. pneumoniae
* N. meningitidis
* L. monocytogenes

381
Q

Where does meningioma arise from

A

Meningothelial cells of the arachnoid layer (arachnoid-cap cells)

382
Q

Compare CSF features of bacterial vs viral meningitis

A

Bacterial
* Opening pressure: raised
* Appearance: turbid, cloudy, purulent
* CSF WBC count: raised (typically >100)
* Predominant cell type: neutrophils
* CSF protein: raised
* CSF glucose: very low
* CSF/plasma glucose ratio: very low

Viral
* Opening pressure: normal/mildly raised
* Appearance: clear
* CSF WBC count: raised (typically 5 to 1000)
* Predominant cell type: lymphocytes
* CSF protein: normal/mildly raised
* CSF glucose: normal
* CSF/plasma glucose ratio: normal

383
Q

Give the meningococcal disease antibiotic prophylaxis

A

oral ciprofloxacin single dose

384
Q

List the symptoms for meningitis

A

Headache
Neck stiffness
Photophobia
Fever
Altered consciousness
Rash
Seizures
Shock

385
Q

Describe Kernig’s and Brudzinski’s sign

A

Kernig’s sign (present in only 11%)
Pain in the lower back or back of thigh on extension of knee when hip is flexed to a 90° right angle

Brudzinski’s sign (present in only 9%)
Forced flexion of the neck elicits a reflex flexion of the hip

386
Q

Give the first line investigation in meningitis

A

Blood culture

387
Q

List the serum electrolyte features in meningitis

A

Acidosis
Hypokalaemia
Hypocalcaemia
Hypomagnesaemia
Low sodium (TB meningitis)

388
Q

List the contraindications for lumbar puncture

A

Signs suggesting raised ICP
Shock
Extensive or spreading purpura
After convulsions, until stabilised
Coagulation abnormalities
Local infection at the lumbar puncture site
Respiratory insufficiency

389
Q

Give the antibiotics in meningitis

A

IM/IV benzylpenicillin (children, adults)
IV ceftriaxone/cefotaxime (adults)

390
Q

List the causes of encephalitis

A

(Viruses)
Herpes viruses
* Herpes simplex virus
* Varicella zoster virus
* Cytomegalovirus
* Epstein-Barr virus
West Nile virus
Picornaviridae / enteroviruses
* Coxsackievirus
* Poliovirus
Bacterial
* Neisseria meningitidis (meningoencephalitis)
* Syphilis
* Listeria
* Bartonella (cat-scratch disease)
* Borrelia burgdorferi (Lyme disease)
Autoimmune
* Anti-NMDA encephalitis
* Acute hemorrhagic leukoencephalitis

391
Q

Give the signs and symptoms in encephalitis

A

Acute/subacute onset of a febrile illness
Altered mental status
Focal neurological abnormalities
Seizures

392
Q

Give the diagnostic criteria for encephalitis

A

Major criteria (required):
Altered mental status lasting ≥24 hours with no alternative cause identified
* Altered level of consciousness
* Lethargy
* Personality change
Minor criteria (2 required for possible, ≥3 required for probable/confirmed encephalitis)
* Documented fever ≥38°C within the 72 hours before/after presentation
* Generalised/partial seizures not fully attributable to a pre-existing seizure disorder
* New onset of focal neurological findings
* CSF WBC count ≥5/mm³
* Abnormality of brain parenchyma on neuroimaging suggestive of encephalitis
* Abnormality on EEG consistent with encephalitis and not attributable to another cause.

393
Q

Give the empirical treatment for encephalitis

A

Immunocompetent - Aciclovir
Immunocompromised - Aciclovir AND ganciclovir AND foscarnet

394
Q

List the symptoms and signs in brain abscess

A

Symptoms
* Recent unexplained fever with neurological deficit
* Headache
* Fever
* New-onset neurological deficits

Signs
* Nuchal rigidity, and Kernig and Brudzinski signs in the presence of neurological deficits
* Increased intracranial pressure and impending cerebral herniation:
* CN3 / 6 palsies
* Anisocoria
* Papilloedema

395
Q

List the most common aetiology for brain abscess by age

A

Neonates - Proteus mirabilis and Citrobacter species
Children - Streptococcus species in combination with cyanotic heart disease
Adults - Streptococcus and Staphylococcus species

396
Q

Give the antibiotic of choice in brain abscess

A

Vancomycin + Metronidazole/clindamycin + third generation cephalosporin (ceftriaxone, cefotaxime)

397
Q

Give the neuroimaging sign in brain abscess

A

1 or more ring-enhancing lesions

398
Q

Give the triad in normal pressure hydrocephalus

A

Clinical features of hydrocephalus without significantly elevated CSF
* levodopa-unresponsive gait apraxia
* urinary incontinence
* cognitive impairment

399
Q

List the cardinal features of levodopa-unresponsive gait apraxia

A

A slow, cautious gait
Gait initiation failure
Unsteadiness
Reduced stride length
Shuffling gait
Falls
Freezing

400
Q

How much CSF is produced by the choroid plexus and is reabsorbed at the arachnoid granulations every minute.

A

0.5 mL

401
Q

List the investigations for normal pressure hydrocephalus

A

MRI/CT without contrast
* May be normal
* Moderate dilation of the ventricles and periventricular leukomalacia
* Disproportionate central atrophy, resulting in larger ventricles with relative preservation of cortical sulci
Levodopa challenge - unresponsive
Lumbar puncture - Normal CSF pressure

402
Q

Give the management for normal pressure hydrocephalus

A

Ventriculoperitoneal shunt surgery

403
Q

List the complications of ventriculoperitoneal shunt surgery

A

subdural haematoma
mechanical obstruction
infection

404
Q

What features of migraine is more common in children?

A

Nausea, vomiting and abdominal pain

405
Q

What are the first-line treatments for spasticity in multiple sclerosis

A

Baclofen and gabapentin

406
Q

Give the diagnosis for seizure after acute sinusitis PLUS:
* Focal Neurology
* Cranial Nerve Palsy, Ophthalmoplegia
* Neck Stiffness, Photophobia, Kernig’s/Brudzinski’s positive
* Painful Ophthalmoplegia, Proptosis, Eye swelling
* Staph. Aureus

A

Focal Neurology - Cerebral Abscess
Cranial Nerve Palsy, Ophthalmoplegia - Cavernous Sinus Thrombosis
Neck Stiffness, Photophobia, Kernig’s/Brudzinski’s positive - Meningitis
Painful Ophthalmoplegia, Proptosis, Eye swelling - Orbital Cellulitis
Staph. Aureus - Frontal bone osteomyelitis

407
Q

What is a contraindication to triptan use

A

Cardiovascular disease

408
Q

List the adverse effects of Lamotrigine

A

Stevens-Johnson syndrome and toxic epidermal necrolysis
Drug reaction with eosinophilia and systemic symptoms (DRESS)

409
Q
A
410
Q

Give the presentation of Stevens-Johnson syndrome after lamotrigine

A

Develops up to 2 months after starting an anti-convulsant.
Usually prodromal illness which resembles a viral upper respiratory tract infection
Followed by rapid onset of painful red skin rash which starts on the trunks and extends abruptly onto the face and limbs.
Rash rarely affects the scalp, palms or soles.

411
Q

When is carotid endarterectomy considered for TIA

A

carotid artery stenosis >50% (NASCET criteria) on the side contralateral to the symptoms

412
Q

What does DVLA say about epilepsy

A

The person with epilepsy may qualify for a driving licence if they have been free from any seizure for 1 year.

413
Q

What drug is used to prevent vasospasm in aneurysmal subarachnoid haemorrhages

A

Nimodipine

414
Q

What is Ondansetron selective for

A

5-HT1 antagonist

415
Q

What is the first line management in pituitary apoplexy

A

IV hydrocortisone

416
Q

List the order of drugs to give in status epilepticus

A
  1. Buccal midazolam/IV lorazepam
  2. IV lorazepam
  3. IV phenytoin/levetiracetam/sodium valproate
  4. Rapid sequence induction of anaesthesia using thiopental sodium
417
Q

What can be used to differentiate a general tonic-clonic/partial seizure from a non-epileptic pseudo seizure

A

Elevated serum prolactin 10 to 20 minutes after an episode

418
Q

Give the first line treatments for neuropathic pain

A

amitriptyline, duloxetine, gabapentin, pregabalin

419
Q

List the causes for neuropathic pain

A

diabetic neuropathy
post-herpetic neuralgia
trigeminal neuralgia
prolapsed intervertebral disc

420
Q
A

Medicine (8 decks)

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