Neurosciences Flashcards

USMLE (428 cards)

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
List the presentations by cerebellar vermis lesions
Truncal ataxia (difficulty standing and sitting unsupported) Broad-based, ataxic gait
26
List the presentations by Flocculonodular region lesions
Vertigo and vomiting Gait ataxia
27
List the causes for an ischaemic stroke (85% cases)
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
28
List the causes for an haemorrhagic stroke (15% cases)
Intracerebral haemorrhage - Hypertension Subarachnoid haemorrhage * Intracranial aneurysm rupture * Arteriovenous malformations * Arterial dissections * Anticoagulant use
29
List the complications in the early period following stroke
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
30
Describe the presentations of a TIA
Neurological dysfunction < 24 hours Unilateral weakness/sensory loss Dysphasia Ataxia, vertigo, loss of balance Syncope Amaurosis fugax, diplopia, homonymous hemianopia Cranial nerve deficits
31
List the risk factors for stroke
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
32
What increases the risk of stroke in female population
Combined oral contraceptives Immediate postpartum period Pre-eclampsia
33
List 4 risk factors for cerebral venous thrombosis
Pregnancy Infection Dehydration Malignancy
34
List the components of the Glasgow Coma Scale
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
35
List the immediate examinations performed in stroke
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
36
Give the immediate management of a suspected TIA
Aspirin 300 mg immediately * PPI cover if dyspepsia * Clopidogrel if aspirin contraindicated
37
Give the management for secondary prevention of stroke
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
38
In which patients non-contrast head CT should be performed within 1 hour?
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
39
Give features on a non-contrast CT head for an ischaemic stroke
hypoattenuation (darkness) of the brain parenchyma loss of grey-white matter differentiation, sulcal effacement hyperattenuation (brightness) in an artery indicates clot
40
What laboratory studies should be indicated in an ischaemic stroke
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.
41
Give the managements in an ischaemic stroke
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).
42
Give the most common cause of intracerebral haemorrhage
Chronic hypertension resulting in * Rupture of microaneurysms (Charcot–Bouchard aneurysms) * Degeneration of small, deep, penetrating arteries
43
List the Nonhypertensive Causes of Intracerebral Haemorrhage
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
44
Give the non-contrast CT imaging features for an intracerebral haemorrhage
hyperattenuation (brightness), suggesting acute blood, often with surrounding hypoattenuation (darkness) due to oedema
45
List 4 causes for a nontraumatic subarachnoid haemorrhage
Aneurysm rupture (80%) Arteriovenous malformations Arterial dissections Anticoagulant use
46
List the symptoms for a subarachnoid haemorrhage
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
47
Give the non-contrast CT imaging features for a subarachnoid haemorrhage
Presence of hyperdense appearance of blood in the subarachnoid space / basal cisterns
48
List two differentials for a sudden onset of severe headache and an elevated CSF opening pressure
cerebral venous sinus thrombosis idiopathic intracranial hypertension
49
What may a sudden onset of severe headache and a reduced CSF opening pressure suggest
low pressure headache
50
List two cardiac complications from an aneurysm rupture
Left ventricular subendocardial injury Takotsubo cardiomyopathy
51
List the investigations and findings after a subarachnoid haemorrhage
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
52
Give the immediate medical management for SAH
Oral nimodipine
53
List the management approaches towards an intracerebral haemorrhage
IV mannitol - reduce ICP Stop / reverse anticoagulation BP control < 140 mmHg systolic Surgical eg. EVD
54
List the signs of rebleeding after SAH
Sudden drop in conscious level Spike in blood pressure Tonic/extensor posturing Pupillary changes
55
List the management approaches for rebleeding after SAH
Early aneurysm repair Short-term Tranexamic acid
56
What are the short term complications after SAH
Rebleeding Acute hydrocephalus Seizures Vasospasm and delayed cerebral ischaemia
57
Give signs of an acute hydrocephalus after SAH
A gradually worsening level of arousal with relative preservation of deliberate motor responses Severe headache/vomiting/agitation
58
Give a management approach for acute hydrocephalus after SAH
CSF drainage or diversion
59
Give signs for a vasospasm and delayed cerebral ischaemia after SAH
≥ 2 drop in GCS score New focal neurological deficit (e.g., unilateral motor or sensory loss, speech disturbance, visual field loss)
60
List the management approaches in vasospasm and delayed cerebral ischaemia after SAH
Triple-H (uses hypertension, hypervolaemia, and haemodilution) Endovascular strategies (balloon angioplasty / intra-arterial vasodilators)
61
List the risk factors for cerebral aneurysms
Hereditary connective tissue diseases: * ADPKD * Neurofibromatosis type 1 * Ehlers-Danlos syndrome type IV * Marfan’s syndrome Hypertension Arteriovenous malformations/fistulas Smoking, Alcohol, Drug abuse
62
List the causes for subdural haematoma
Trauma (most common) Rupture of a cerebral aneurysm Vascular malformation * AVM * Dural fistula
63
What does acute SDH typically result from?
torsional / shear forces causing disruption of bridging cortical veins
64
List the CT appearances in SDH
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
65
List the signs of a skull base fracture
Raccoon eyes CSF rhinorrhea CSF otorrhea Haemotympanum
66
Give the typical time line in extradural haemorrhage
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
67
List the differential diagnoses for dementia syndrome
Normal-age related memory changes Mild cognitive impairment Depression Delirium Thiamine deficiency (Wernicke-Korsakoff’s syndrome) Hypothyroidism Normal pressure hydrocephalus
68
List the risk factors for dementia syndrome
Age Mild cognitive impairment (MCI) Learning disability Genetics Cardiovascular disease Cerebrovascular disease Parkinson's disease (PD)
69
List the causes for dementia syndrome
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
70
Name two pathological findings in Alzheimer's disease
extracellular plaques composed primarily of amyloid intraneuronal neurofibrillary tangles composed primarily of hyperphosphorylated tau
71
List the specific features for Alzheimer's disease
Loss of recent memory first Difficulty with executive function / nominal dysphasia Loss of episodic memory Cognitive deficits - aphasia, apraxia, agnosia
72
List the management for Alzheimer's disease
Acetylcholinesterase (AChE) inhibitors - mild to moderate AD * Donepezil * Rivastigmine * Galantamine Memantine (N-methyl-D-aspartic acid receptor antagonist) - moderate to severe AD
73
List the causes for vascular dementia
Large / multiple small infarcts Haemorrhage Cerebral amyloid angiopathy Subcortical leukoencephalopathy
74
List the specific features in vascular dementia
Stepwise increase in severity of symptoms Focal neurological signs eg. hemiparesis / visual field defects
75
List the specific features for Dementia with Lewy Bodies
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
76
Give the first line management in Dementia with Lewy Bodies
donepezil or rivastigmine
77
List four conditions which Frontotemporal dementia maybe associated with
Amyotrophic lateral sclerosis (ALS) Parkinsonism Corticobasal degeneration Progressive supranuclear palsy
78
What drugs should FTD not be offered with
AChEi Memantine
79
List the diagnostic criteria for delirium
Evident disturbance in attention Cognitive change Develops over a short period of time Evident physiological disturbance
80
Give three clinical subtypes of delirium
Hyperactive Hypoactive Mixed
81
List the common causes of delirium
PINCHME: Pain Infection Nutrition Constipation deHydration Medication Environment
82
Give the pathophysiology of migraine
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.
83
Give key features of migraine
Intermittent Headache Visual disturbance Nausea and vomiting Photophobia and phonophobia Reduced ability to function
84
List the management approaches to migraine
aspirin (900 mg) sumatriptan
85
List the medication for prophylaxis in migraine
propanolol
86
List the triggers for tension type headache
Psychological stress (most common) Disturbed sleep patterns (episodic) Insomnia and other sleep disorders (chronic)
87
Describe the clinical features in tension headache
Dull, non-pulsatile pain (typically expressed as being a 'tight band' around the head)
88
list the medication for an acute attack of tension headache
Aspirin
89
What may cluster headache be precipitated by?
Alcohol Volatile smells Warm temperatures Sleep
90
List three cardinal features in cluster headache
Trigeminal distribution of the pain Ipsilateral cranial autonomic symptoms Circadian/circannual pattern of attacks
91
Give the International Headache Society (IHS) diagnostic criteria for cluster headache
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.
92
Give the acute attack therapy in cluster headaches
subcutaneous sumatriptan / nasal zolmitriptan High flow oxygen
93
Give the preventative therapy in cluster headaches
Verapamil
94
Give the symptom in trigeminal neuralgia
Unilateral paroxysms of facial pain lasting seconds to minutes in a distribution along ≥1 divisions of the CNV
95
Describe the pathophysiology in trigeminal neuralgia
Neuropathic pain due to focal demyelination and resultant conduction aberration
96
List the triggers for trigeminal neuralgia
Tooth brushing Eating Cold Touch
97
Give the medical management in trigeminal neuralgia
Carbamazepine Oxcarbazepine
98
Give one complications for giant cell arteritis
irreversible vision loss due to optic nerve ischaemia
99
List the presentations in giant cell arteritis
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
100
Give the medical management in giant cell arteritis
IV high-dose methylprednisolone
101
Give the histological features in giant cell arteritis
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
102
List the spinal reflex arcs and their levels
S1-2 Ankle L3-4 Knee jerk C5-6 Biceps C7-8 Triceps
103
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) 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.
104
List the presentations in central cord syndromes
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
105
List the presentations in anterior cord syndromes
(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
106
List the presentations in posterior column syndrome
Loss of vibration and proprioception Spastic paraparesis and brisk reflexes Urgency and incontinence Retained pain and temperature sensation
107
List the presentations in syringomyelia
‘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
108
List the causes for spinal cord compression
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
109
List the signs for cervical spondylotic radiculopathy
Radiating arm pain Mild weakness in the muscles Reflex changes
110
List the signs for degenerative cervical myelopathy
Loss of hand coordination Hand intrinsic muscles weakness eg. interossei Mild gait ataxia (impaired position sense) Bowel and bladder difficulties in severe cases
111
List the metastatic causes for malignant spinal cord compression
Prostate Breast Lung Renal Thyroid
112
List the lab tests ordered in malignant spinal cord compression
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
113
List the afferent and efferent pupillary light reflex pathway
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
114
List the signs of a left APD
Absent direct and consensual reflex Intact consensual reflex of the right eye
115
What does an incomplete damage to one optic nerve relative to the other cause?
Relative afferent pupillary defect
116
What is internuclear ophthalmoplegia caused by
lesion of the medial longitudinal fasciculus
117
List the major cause of internuclear ophthalmoplegia
Multiple sclerosis
118
List the signs of internuclear ophthalmoplegia
Ipsilesional adduction deficit Contralateral, horizontal abducting nystagmus on attempted gaze to the contralesional side
119
List the signs of large vestibular schwannoma
Headache CN5 compression * Hemifacial hypo/paraesthesia * Trigeminal neuralgia CN7 compression - Facial spasm/weakness 4th ventricle compression - Obstructive hydrocephalus Cerebellar displacement * Nystagmus * Ataxia
120
List the central and peripheral causes of vertigo
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
121
List the vestibular migraine features
vertigo visual disorders occipital pressure nausea and vomiting
122
Give the major mechanisms of all subtypes of BPPV
Canalithiasis
123
Give the major mechanism of lateral canal BPPV
Cupulolithiasis
124
List the secondary causes of BPPV
Head trauma Labyrinthitis Vestibular neuronitis Meniere's disease (endolymphatic hydrops) Migraines Ischaemia Iatrogenic
125
List the subtypes of BPPV
Posterior canal Lateral canal Superior canal
126
Give the presentation of BPPV
Sensation that the environment is spinning around relative to oneself Sudden onset and intense vertigo Precipitated by head movements Short duration Episodic and recurrent
127
What does the Dix-Hallpike manoeuvre test for?
Posterior canal BPPV
128
Describe the Dix-Hallpike manoeuvre
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°
129
Describe the Dix-Hallpike manoeuvre findings in right sided BPPV
Eyes rotate in an anticlockwise manner during the fast phase of nystagmus With a slight up-beating vertical component (towards the forehead)
130
Describe the Dix-Hallpike manoeuvre findings in left sided BPPV
Eyes rotate in a clockwise manner during the fast phase of nystagmus With a slight up-beating vertical component (towards the forehead)
131
What does supine lateral head turns test for
lateral canal BPPV
132
Give the hallmark feature in lateral canal BPPV, when tested by supine lateral head turns
pure horizontal nystagmus without a torsional (rotatory) component
133
List the signs of canalithiasis, when tested by supine lateral head turns
horizontal nystagmus with the fast phase beating towards the ground (geotropic) the side with the stronger response is the affected side
134
List the signs of cupulolithiasis, when tested by supine lateral head turns
the fast phase beats away from the ground (apogeotropic) the side with the weaker response is the affected side
135
Give the management for BPPV
Particle repositioning manoeuvre
136
Define Meniere's disease
Endolymphatic hydrops - overproduction or impaired absorption of endolymph
137
Give the classic presentation in Meniere's disease
Episodic sudden onset of vertigo, hearing loss, tinnitus, and sensation of fullness in the affected ear.
138
List the signs in Meniere's disease
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
139
List the management options in Meniere's disease
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
140
Define Labyrinthitis
Inflammation of the otic capsule: * Cochlea * Three orthogonal semi-circular canals * Otolith organs (utricle, saccule)
141
What does suppurative (bacterial) labyrinthitis present with
severe to profound hearing loss (typically irreversible) and vertigo
142
What is suppurative (bacterial) labyrinthitis associated with?
(Direct microbial invasion of the inner ear) Acute/chronic otitis media Cholesteatoma Meningitis
143
List the potential bacterial causes in suppurative (bacterial) labyrinthitis
Treponema pallidum Haemophilus influenzae Streptococcus species Staphylococcus species Neisseria meningitidis
144
What does serous (viral) labyrinthitis present with
less severe hearing loss (often reversible) and vertigo than suppurative labyrinthitis.
145
Is suppurative (bacterial) labyrinthitis more common in adults or children
adults
146
What is serous (viral) labyrinthitis associated with
Preceding URTI Autoimmune inner ear disease * Cogan's syndrome * Behçet’s disease
147
List the viral agents involved in serous (viral) labyrinthitis
Varicella zoster virus Cytomegalovirus Mumps, measles, rubella HIV
148
List the presentations in labyrinthitis
Unilateral sensorineural hearing loss Tinnitus Vertigo with nausea and vomiting
149
List the signs in labyrinthitis
Spontaneous horizontal-rotary nystagmus - fast phase beating towards the normal ear Significant difficulty walking Unable to perform tandem gait Fall with Romberg’s testing
150
List the causes of vestibular neuronitis
Inflammation of the vestibular nerve (after a viral infection) Secondary to ischaemia of the anterior vestibular artery
151
How to differentiate vestibular neuronitis with labyrinthitis
hearing is not affected in vestibular neuronitis.
152
List the complications in vestibular neuronitis
BPPV Persistent postural perceptual dizziness (PPPD) Oscilloposia
153
List the presentations in vestibular neuronitis
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
154
Give the ocular sign in vestibular neuronitis
Nystagmus with the fast phase away from the affected ear
155
Give the symptomatic managements for nausea, vomiting, vertigo in vestibular neuronitis
Buccal prochlorperazine Intramuscular prochlorperazine / cyclizine
156
List the four characteristic features of Parkinsonism
Bradykinesia Tremor Rigidity Postural instability
157
List the causes of Parkinsonism
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
158
List the drugs that may cause Parkinsonism
First generation antipsychotics (fluphenazine, trifluoperazine, haloperidol, chlorpromazine, flupentixol, zuclopenthixol) Antiemetics (prochlorperazine, metoclopramide)
159
List the symptoms in multiple system atrophy
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
160
List the symptoms of progressive supranuclear palsy
Parkinsonism Early dysphagia Vertical gaze palsy Recurrent falls (postural instability)
161
List the symptoms of corticobasal degeneration
Parkinsonism Asymmetric rigidity and dystonia Cortical sensory loss Progressive aphasia Apraxia Cognitive impairment Alien limb phenomenon
162
List the symptoms of Wilson's disease
Kayser-Fleischer rings Variable neurological signs including tremor, ataxia, dystonia Non-specific liver disease
163
List the symptoms in Parkinson's disease
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
164
List the pathologies in Parkinson's disease
Selective loss of nigrostriatal dopaminergic neurons in the substantia nigra pars compacta (SNc) Intracytoplasmic eosinophilic inclusions (Lewy bodies) and neurites, composed of alpha-synuclein
165
Give the pathophysiology in Parkinson's disease
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
166
List the symptomatic management options in Parkinson's
Levodopa Monoamine oxidase-B (MAO-B) inhibitors * Selegiline * Rasagiline * Safinamide Dopamine agonists * Pramipexole (oral) * Ropinirole (oral) * Rotigotine (transdermal)
167
List the side effects of levodopa
Dyskinesia Excessive sleepiness Hallucinations Impulse control disorders
168
List the causes of tremor
Essential tremor Postural and action tremor * Dystonic tremor * Hyperthyroidism * Drugs eg. beta2-agonists Intention tremor - cerebellar disorder
169
List the presentations in essential tremor
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
170
List the presentations in Huntington's disease
Chorea Incoordination Cognitive decline Personality changes Psychiatric symptoms
171
List the causes of chorea
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
172
List the management options for depression in Huntington's disease
Fluoxetine (SSRI) Buspirone Benzodiazepines
173
Give the inheritance and genetic mechanism in myoclonic dystonia
Autosomal dominant disorder Mutation in ε-sarcoglycan gene
174
List the characteristics in Tourette’s syndrome
Childhood onset Motor and vocal tics Psychiatric disorders (OCD, ADHD)
175
Give the first line management for tics in Tourette’s syndrome
Comprehensive behavioural intervention for tics
176
List the pharmacological therapies in Tourette’s syndrome
Alpha-2 agonist (monotherapy at minimal dosage) * Clonidine * Guanfacine Antipsychotics * Aripiprazole * Risperidone * Ziprasidone Botulinum toxin
177
Define geste antagoniste
Dystonia may improve with simple 'sensory tricks' such as lightly touching the affected body part
178
List the presentations in focal dystonia
Axial * Blepharospasm * Cervical torticollis Limb * Task related (writer’s cramp) * Foot * Orofacial/mandibular
179
Give one cause of early-onset (<26 years) dystonia
TOR1A gene mutations
180
List the management options of generalised dystonias
Levodopa Trihexyphenidyl (anticholinergic) Pallidal deep brain stimulation
181
List the four clinical patterns of motor neurone disease
Amyotrophic lateral sclerosis Progressive muscular atrophy Progressive bulbar and pseudobulbar palsy Primary lateral sclerosis
182
List the presentations in progressive muscular atrophy
Pure LMN presentation Weakness Muscle wasting Fasciculations Usually starting in one limb and gradually spreading to involve other adjacent spinal segments
183
List the presentations of primary lateral sclerosis
UMN disorder Slowly progressive tetraparesis and pseudobulbar palsy
184
List the UMN signs
Mild weakness Spasticity Hyperreflexia and clonus Pathological reflexes: * Babinski * Hoffmann sign * Loss of abdominal reflexes
185
List the LMN signs
Moderate to severe weakness Atrophy Hyporeflexia Flaccidity Fasciculations
186
List the aetiologies in ALS
Sporadic (mostly) Genetic * free radical scavenging enzyme superoxide dismutase (SOD-1) - missense mutations * C9orf72 * TDP-43 * FUS
187
List the initial symptoms in ALS
Isolated dysarthria Hand weakness Foot drop Gait changes Shortness of breath
188
What is familial ALS associated with
FTD
189
List the physical examination findings in ALS
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
Give the diagnostic criteria in ALS
(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
List the investigations for ALS
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
List other tests to exclude in ALS
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
Give the 1st line and alternative Disease-modifying pharmacological therapies for ALS
1st line: Riluzole Edaravone (antioxidant) Sodium phenylbutyrate / tauroursodeoxycholic acid
194
Give the mechanism of Riluzole
Glutamate inhibitor, reduces excitotoxicity
195
Give two adverse effects associated with riluzole
Hepatotoxicity and neutropenia (rare) LFT and FBC monthly for first 3 months, then every 3 months
196
Give the mutation in DMD and Becker muscular dystrophy
Dystrophin - exon deletions
197
Give the inheritance of DMD
X-linked recessive
198
What do the mutations in Emery-Dreifuss muscular dystrophy affect
Nuclear envelope proteins * Emerin (X-linked recessive) * Lamin A/C (autosomal dominant)
199
Give the mutations in Facioscapulohumeral muscular dystrophy
Small deletion on chromosome 4 affecting D4Z4 region in FSHD1 (95%) SMCHD1 region in FSHD2
200
Give the inheritance in Facioscapulohumeral muscular dystrophy
Autosomal dominant Spontaneous mutations (up to 30%)
201
Give the mutation in Myotonic dystrophy type 1 (DM1)
CTG triplet repeat expansion in the 3' non-coding region of DMPK
202
Give the onset age for Limb-girdle muscular dystrophies
10~20 years
203
Give the onset age for Facioscapulohumeral muscular dystrophy
10–40 years
204
What muscles are predominantly affected in Limb-girdle muscular dystrophies
Proximal: shoulders, pelvic girdle
205
What muscles are predominantly affected in facioscapulohumeral muscular dystrophies
Face, shoulders, scapular winging, upper arms, foot drop. Typically asymmetric
206
What are the associated features in facioscapulohumeral muscular dystrophies
deafness and retinal abnormalities
207
Give the prognosis in Limb-girdle muscular dystrophies
Severe disability <25 years
208
Give the prognosis in facioscapulohumeral muscular dystrophies
Life expectancy normal, slow progression
209
Give the pathophysiology in DMD
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
List the classic presentation in Duchenne muscular dystrophy
Toddler with * Delayed motor milestones * Calf hypertrophy * Proximal hip girdle muscle weakness * Marked elevation of serum creatine kinase
211
List the physical examination findings in Duchenne muscular dystrophy
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
List the management options for DMD
Corticosteroid therapy - Preserve muscle strength Prevention/reduction of musculotendinous contractures Physiotherapy
213
List the novel oral direct factor Xa inhibitors
Apixaban Betrixaban Edoxaban Rivaroxaban
214
List the novel oral direct factor IIa inhibitors
Dabigatran
215
List the presentations in Anterior cerebral artery syndrome
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
List the presentations in infarction of the Inferior division of dominant MCA
Contralateral homonymous hemianopia or upper quadrant anopsia Receptive aphasia (Wernicke)
217
List the presentations in infarction of the superior division of dominant MCA
Contralateral weakness (affects the lower face and arm more than the leg) Contralateral sensory loss (including the face) Contralateral hemineglect Expressive aphasia (Broca)
218
List the presentations in infarction of the Whole of the dominant MCA
(Gerstmann syndrome) Agraphia, Acalculia, Finger agnosia Right-left disorientation Contralateral weakness, sensory loss Contralateral hemineglect Contralateral homonymous hemianopia Global aphasia (receptive and expressive)
219
List the signs of elevated ICP
Reducing level of consciousness Severe headache Nausea/vomiting Sudden increase in blood pressure
220
Give the presentations in occlusion of one of the paramedian branches of the basilar artery
Weber syndrome (Ventromedial midbrain) * Ipsilateral oculomotor nerve palsy * Contralateral hemiplegia
221
Give the presentations in Anterior inferior cerebellar artery (AICA) infarction
(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
List the presentations in Posterior inferior cerebellar artery (PICA) infarction
(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
Give the transitional therapy options in cluster headache
Prednisolone IV dihydroergotamine (Contraindicated in patients with CV risk factors (CAD, HTN)) Greater occipital nerve block
224
List the severity grading and mortality in TBI
Mild TBI: GCS 13-15; mortality 0.1% Moderate TBI: GCS 9-12; mortality 10% Severe TBI: GCS <9; mortality 40%
225
List the aetiologies for TBI
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
What is Diffuse axonal injury
Rapid rotational/deceleration force that causes stretching and tearing of neurons, followed by focal areas of haemorrhage and oedema.
227
List the CT grading for Diffuse axonal injury
Petechial haemorrhages and oedema located at the: Grey-white matter junction (Grade 1) Corpus callosum (Grade 2) Brainstem (Grade 3)
228
List the primary interventions to elevated intracranial pressure
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
List the secondary interventions to elevated intracranial pressure
Osmosis: hypertonic saline, mannitol High-dose barbiturate ICP monitoring Decompressive hemicraniectomy
230
List the six cognitive domains
attention executive function memory and learning language perceptual motor social cognition
231
Give the DSM5 diagnostic criteria for Major Neurocognitive Disorder/Dementia
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
Define Idiopathic intracranial hypertension
Increased intracranial pressure in an alert and oriented patient
233
In what population does Idiopathic intracranial hypertension predominantly occur?
overweight women of childbearing years, often in the setting of weight gain.
234
Give the pathophysiology in Idiopathic intracranial hypertension
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
List the symptoms and signs of Idiopathic intracranial hypertension
Symptoms * Headaches * Pulse-synchronous tinnitus * Transient visual obscurations, visual loss, diplopia * Neck and back pain Signs * Papilloedema * CN6 paresis * Sensory visual disturbances
236
List the secondary causes of intracranial hypertension
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
List the investigations and findings in Idiopathic intracranial hypertension
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
List the non-medical management options for Idiopathic intracranial hypertension
Weight-reduction Low-sodium diet
239
List the medical management options for Idiopathic intracranial hypertension
Acetazolamide Furosemide Topiramate
240
List the mechanisms of Acetazolamide in treating Idiopathic intracranial hypertension
Inhibit carbonic anhydrase, reduces sodium ion transport across the choroid plexus epithelium Acetazolamide decreases CSF production in humans by 6~50%
241
List the contents in cavernous sinus
CN III, IV, V1, V2, VI Internal carotid artery
242
List the sources of cavernous sinus
Superior and Inferior ophthalmic vein Superficial middle cerebral vein Middle meningeal vein Hypophyseal veins
243
Where does cavernous sinus drain to
Superior and inferior petrosal sinuses
244
List the septic causes of Cavernous sinus thrombosis
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
List the aseptic causes of Cavernous sinus thrombosis
Trauma Post-surgery Hypercoagulable states Malignancy * Rhabdomyosarcoma * Nasopharyngeal carcinoma Vascular abnormalities
246
List the Hypercoagulable states
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
What is the most common causative organism for septic Cavernous sinus thrombosis
Staphylococcus aureus
248
List the causative organisms in septic Cavernous sinus thrombosis
Staphylococcus aureus (most common) Fusobacterium necrophorum Streptococci
249
List the presentations in Cavernous sinus thrombosis
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
Give the investigation and finding in Cavernous sinus thrombosis
CT with contrast - abnormal filling defects with lateral convexity of the cavernous sinuses
251
List the managements in Cavernous sinus thrombosis
Empirical antibiotics: vancomycin with/without rifampicin Linezolid Trimethoprim/sulfamethoxazole
252
Give the level of motor lesion in bulbar palsy and pseudobulbar palsy
Bulbar - LMN Pseudobulbar - UMN
253
List the clinical features in bulbar palsy
Tongue - wasted, fasciculations Absent palatal movement Absent gag reflex Absent jaw jerk Nasal speech (flaccid dysarthria) Normal emotions
254
List the causes of bulbar palsy
Motor neurone disease Syringobulbia Guillain-Barre syndrome Poliomyelitis Subacute menignitis (carcinoma, lymphoma) Neurosyphilis Brainstem cerebrovascular accident
255
What is the most common cause for pseudobulbar palsy
Bilateral cerebrovascular accidents affecting the internal capsule
256
List the causes for pseudobulbar palsy
Cerebrovascular accidents Multiple sclerosis Motor neurone disease High brainstem tumours Head injury
257
List the clinical features in pseudobulbar palsy
Spastic tongue, slow moving Absent palatal movement Increased gag reflex Increased jaw jerk Spastic speech, ‘Donald Duck’ dysarthria Labile emotions
258
Describe the gait in Parkinson’s disease and other Parkinsonian syndromes
Stooped posture Shuffling (reduced stride length) Loss of arm swing Postural instability Freezing
259
Describe the gait in muscular dystrophies and acquired myopathies
(Myopathic gait) Waddling (proximal weakness) Bilateral Trendelenburg signs
260
Describe the gait in common peroneal nerve palsy
Foot drop
261
Describe the gait in cerebellar disease
(Central ataxia) Wide-based, ‘drunken’ Tandem gait poor
262
Describe the gait in sensory ataxia
Wide-based Positive Romberg sign
263
List the causes of positive Romberg sign
Sensory ataxia Bilateral vestibular failure
264
Describe the gait in Hemiplegia
The foot on the affected side is plantar flexed and describes a semicircle as the patient walks The upper limb may be flexed
265
Describe the gait in bilateral UMN damage
Scissor-like gait (spasticity)
266
List the drugs commonly causing tremor
Sodium valproate Glucocorticoids Lithium
267
Describe the tremor in Parkinson’s disease
slow (3 to 7 Hz), coarse, ‘pill-rolling’ tremor, worse at rest but reduced with voluntary movement
268
Describe Physiological tremor
fine (low-amplitude), fast (high-frequency, 3 to 30 Hz) postural tremor
269
List the Medical Research Council grading of muscle power
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
List the nerve and muscle supplies of shoulder abduction
Deltoid - Axillary C5
271
List the nerve and muscle supplies of: Elbow flexion Elbow extension
Elbow flexion * Biceps - Musculocutaneous C5/6 * Brachioradialis (supinator reflex) - Radial C6 Elbow extension * Triceps - Radial C7
272
List the nerve and muscle supplies of: Wrist extension
Extensor carpi radialis longus - Radial (posterior interosseous branch) C6
273
List the nerve and muscle supplies of: Finger extension Finger flexion
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
List the nerve and muscle supplies of: Finger abduction Thumb abduction
Finger abduction * First dorsal interosseous - Ulnar T1 Thumb abduction * Abductor pollicis brevis - Median T1
275
List the nerve and muscle supplies of: Hip flexion Hip extension
Hip flexion * Iliopsoas - Iliofemoral nerve L1/2 Hip extension * Gluteus maximus - Sciatic L5/S1
276
List the nerve and muscle supplies of: Knee flexion Knee extension
Knee flexion * Hamstrings - Sciatic S1 Knee extension * Quadriceps - Femoral L3/4
277
List the nerve and muscle supplies of: Ankle dorsiflexion Ankle plantar flexion
Ankle dorsiflexion * Tibialis anterior - Common peroneal L4/5 Ankle plantar flexion * Gastrocnemius and soleus - Tibial S1/2
278
List the nerve and muscle supplies of: Great toe extension (dorsiflexion)
Extensor hallucis longus - Common peroneal L5
279
List the nerve and muscle supplies of: Ankle eversion Ankle inversion
Ankle eversion * Peronei - Common peroneal L5/S1 Ankle inversion * Tibialis posterior - Tibial nerve L4/5
280
What may isolated loss of a reflex suggest
mononeuropathy radiculopathy
281
What may unilateral grasp and palmomental reflexes suggest
Contralateral frontal lobe pathology
281
List the causes of Bell's palsy
Ramsay Hunt syndrome (herpes zoster infection of the geniculate (facial) ganglion) Vestibular schwannoma (cerebellopontine angle compression) Parotid tumours Trauma
282
List the features in Bell's palsy
(LMN CN7 paralysis) Weakness of both upper and lower facial muscles Taste impairment Hyperacusis
283
What is anterior cord syndrome caused by
Anterior vertebral artery injury eg. flexion injury
284
What is the most common cause of central recurrent attacks of vertigo
Migraine
285
Give the pathophysiology in cervical spondylotic radiculopathy
Mechanical compression/chemical irritation of a specific nerve root by * degenerative disc * degenerative joint changes, narrowing the root exit at the foraminal level
286
Give the pathophysiology in degenerative cervical myelopathy
Posterior disc protrusion Congenital spinal canal narrowing Osteophytic bars Ligamentous thickening Ischaemia
287
Give the managements in malignant spinal cord compression
Corticosteroid - dexamethasone sodium phosphate Radiotherapy Surgery
288
Give the landmark for conus medullaris
T12-L1
289
Contrast the presentations in cauda equina syndrome vs conus medullaris syndrome
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
List the clinical presentations in cauda equina syndrome
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
Give the investigation for cauda equina syndrome
MRI lumbar spine without IV contrast
292
What diseases may affect the anterior horn cells?
Anterior poliomyelitis Motor neuron disease
293
What may axonal degeneration be caused by
Systemic metabolic disorders Toxin exposure Vasculitis Inherited neuropathies
294
What does axonal degeneration present as
Stocking and glove sensory loss Muscle weakness and atrophy Loss of distal limb myotatic reflexes
295
Give the presentation when anterior horn cells are affected
Focal weakness without sensory loss
296
Give the presentation when dorsal root ganglion neurons are affected
Sensory ataxia Sensory loss Diffuse areflexia
297
What diseases may affect the dorsal root ganglion neuron?
Toxins * organic mercury compounds * doxorubicin * high-dose pyridoxine Vitamin E deficiency Immune-mediated * paraneoplastic sensory neuronopathy * Sjögren syndrome
298
List the types of nerve fibres
Sensory - large myelinated Motor - small myelinated Autonomic - small unmyelinated
299
List the presentations in L5 Radiculopathy
Foot drop Weak ankle inversion
300
List the presentations in Sciatic nerve L4~S3 palsy
Paralysis of knee flexion and all movements below knee Sensory loss below knee Reflexes * ankle and plantar reflex lost * knee jerk intact
301
List the presentations in Tibial nerve L4~S3 palsy
Inability to * Stand on tiptoe (plantar flexion) * Invert the foot * Flex the toe * Sensory loss over the sole
302
Give the Median nerve root
C6-T1
303
What other conditions may be carpal tunnel syndrome be seen in
Hypothyroidism Pregnancy (third trimester) Rheumatoid disease Acromegaly Amyloidosis, including dialysis
304
List the risk factors for carpal tunnel syndrome
variations in the anatomy of the carpal tunnel age over 30 years high BMI pregnancy occupations involving repetitive movements of the wrist
305
List the clinical presentations for carpal tunnel syndrome
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
Give the gold standard investigation in carpal tunnel syndrome and findings
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
Give the ulnar nerve root and list the ulnar neuropathy presentation
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
Give the radial nerve root and list the radial neuropathy presentation
Radial nerve root = C5-T1 Wrist drop Weakness of brachioradialis and finger extension
309
What is meralgia paraesthetica caused by? Give its presentation
Compression of the lateral femoral cutaneous nerve (L2-3) Anterio-lateral burning thigh pain
310
Give the common peroneal nerve root and list the common peroneal neuropathy presentation
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
Name two branches of the sciatic nerve
Divides into tibial and common peroneal nerves
312
In what conditions may mononeuritis multiplex occur in
Vasculitis Diabetes mellitus Malignancy Neurofibromatosis HIV and hepatitis C infection Leprosy Multifocal motor neuropathy with conduction block.
313
Give the presentation in mononeuritis multiplex
Painful, acute to subacute sensory and motor deficits that may be limited to one nerve or multifocal.
314
Give the typical presentations in polyneuropathies
Symmetric numbness, paraesthesias, and dysesthesias in the feet and distal lower extremities. Stocking-glove sensory symptoms in severe cases
315
List the specific etiologies for demyelinating polyneuropathy
Guillain–Barré syndrome Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) Monoclonal gammopathies Hereditary neuropathies
316
List the neuropathies with Autonomic Nervous System Involvement
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
Give the aetiology for Guillain–Barré syndrome
Infections in the 6 weeks before symptom onset Campylobacter jejuni Cytomegalovirus Epstein–Barr virus Mycoplasma pneumoniae
318
List the symptoms and signs in Guillain–Barré syndrome
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
List the investigations and findings in Guillain–Barré syndrome
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
List the management options for Guillain–Barré syndrome
high-dose intravenous immunoglobulin (IVIG) plasma exchange
321
List the causes for Wernicke–Korsakoff’s syndrome
(Thiamine (vitamin B1) deficiency) Alcohol (most common) Anorexia nervosa Vomiting of pregnancy
321
List the physical examination findings in Charcot-Marie-Tooth disease
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
List the presentations in Wernicke–Korsakoff’s syndrome
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
List the key features in Charcot-Marie-Tooth disease
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
Name the most common type of Charcot-Marie-Tooth disease, inheritance, and genetic mechanisms
CMT 1A - most common Autosomal dominant PMP22 gene duplication
321
Define CMT type 1 and CMT2
CMT type 1 (CMT1) - demyelinating conductions and dominant inheritance CMT2 - axonal conductions and dominant inheritance
321
What does dietary deficiency of Thiamine (vitamin B1) cause
beriberi * Polyneuropathy * Cardiac failure
322
Give the typical presentation in Pyridoxine (vitamin B6) deficiency
limb numbness developing during anti-tuberculosis therapy with slow isoniazid acetylators
323
How is Pyridoxine (vitamin B6) deficiency prevented
Prophylactic pyridoxine 10 mg daily is given with isoniazid
324
List the presentations of Vitamin B12 (cobalamin) deficiency
Subacute combined degeneration of the cord (SACD) * spastic paraparesis * loss of vibration sense, proprioception, and two-point discrimination * ataxic gait * reduced sensation
325
Give the pathologies in multiple sclerosis
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
List the four main clinical patterns of MS
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
List the common presenting symptoms in multiple sclerosis
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
List the neurological signs in multiple sclerosis
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
Give the first line investigation and findings in multiple sclerosis
MRI brain (high field magnet with IV gadolinium contrast) * Hyperintensities in the periventricular white matter * Demyelinating lesions in the spinal cord, particularly cervical
330
List the LP findings in MS
Oligoclonal bands CSF IgG
331
Give the management for acute MS relapse
Oral methylprednisolone 0.5 g for 5 days Plasma exchange
332
Give the management for Secondary progressive MS
1st line: Siponimod or IV methylprednisolone 2nd line: Cladribine
333
Give the management for Primary progressive MS
Ocrelizumab
334
List the antibodies for neuromyelitis optica spectrum disorders (NMOSD)
Anti-aquaporin 4 Anti-myelin oligodendrocyte glycoprotein
335
List the NMOSD adult presentations
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
List the typical presentations in transverse myelitis
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
List the treatment for Transverse myelitis
IV methylprednisolone
338
Define Progressive Multifocal Leukoencephalopathy
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
List the causes for Progressive Multifocal Leukoencephalopathy
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
List the presentations for Progressive Multifocal Leukoencephalopathy
New-onset neurological symptoms in a patient with immunosuppression Cognitive impairment Limb, gait ataxia Hemiparesis Hemianopia Aphasia
341
Give the CT findings in Progressive Multifocal Leukoencephalopathy
hypodense confluent lesions without mass effect
342
List the risk factors of essential tremor
Ageing Genetics Environmental toxins * Organochlorine pesticides * Lead * Mercury * Beta-carboline alkaloids (harmane, harmaline)
343
List the management options for essential tremor
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
Give the inheritance and genetic mechanism in Huntington's disease
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
Give the pathology in Huntington's disease
Degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
346
Define Posthypoxic myoclonus
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
List the primary and secondary causes of myoclonus
Primary * Physiological * Myoclonic dystonia * Epilepsy Secondary * Metabolic disorders (hepatic and renal failure, asterixis) * Alzheimer’s * Encephalitis
348
Give the natural history in Tourette’s syndrome
Symptoms typically begin in childhood, peak prior to puberty, attenuate later in adolescence
349
List the causes for restless legs syndrome
Primary - familial, autosomal dominant Secondary * Iron deficiency * Pregnancy (26%, third trimester) * Uraemia * Renal dialysis/ESRD (20%)
350
What is restless legs syndrome associated with
Obesity Diabetes Multiple sclerosis Parkinson's disease Neuropathy
351
What medicines can cause or worsen restless leg symptoms
TCAs, SSRIs Sedating antihistamines Metoclopramide (DPA antagonist) Neuroleptics
352
List the presentations for restless legs syndrome
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
Give the McDonald diagnostic criteria for multiple sclerosis
(Dissemination in both time and space) 2 or more attacks + 2 or more lesions on MRI
354
What population does MS classically present in
White women aged between 20 and 40 years.
355
List the risk factors for MS
EBV infection Female, caucasian, HLA-DRB1 Environmental factors * Location (USA, europe) * Cold climate Low vitamin D Smoking
356
List the differential diagnoses in MS
Thyroid disease Vitamin B12 deficiency Diabetes mellitus
357
List the antibodies positive in myasthenia gravis
Anti-AChR (80-90%) Anti-muscle-specific tyrosine kinase (MuSK) (3-7%)
358
Give the pathophysiology in myasthenia gravis
Circulating antibodies against the nicotinic acetylcholine receptor (AChR) or associated proteins impair neuromuscular transmission.
359
List the clinical features in myasthenia gravis
Muscle weakness that increases with exercise (fatigue) and improves on rest. * Ptosis, Diplopia * Dysarthria, Dysphagia * Facial paresis * Proximal limb weakness * Shortness of breath
360
Define myasthenic crisis
An MG exacerbation requiring mechanical ventilation * forced vital capacity ≤ 15 (normal ≥60 mL/kg) * negative inspiratory force ≤ 20 (normal ≥70 cm H₂O)
361
What may myasthenic crisis be provoked by
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
Give the management in myasthenic crisis
Intubation and mechanical ventilation Plasma exchange / IVIG
363
List the management options for myasthenic crisis
1st line: Pyridostigmine (cholinesterase inhibitor) Prednisolone Azathioprine Rituximab (MuSK-MG) Thymectomy
364
When may thymectomy be considered in MS
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
What conditions are associated with Lambert Eaton syndrome
Small cell lung cancer Autoimmune thyroid disease Vitamin B12 deficiency Rheumatoid arthritis Inflammatory myopathy Systemic vasculitis
366
What is Lambert Eaton syndrome associated with
Small cell lung cancer (CA-LEMS) Autoimmune (NCA-LEMS) * Autoimmune thyroid disease * Vitamin B12 deficiency * Rheumatoid arthritis * Inflammatory myopathy * Systemic vasculitis
367
List the differences between LEMS and MG
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
Give the pathophysiology in LEMS
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
List the symptoms in LEMS
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
List the signs in LEMS
Proximal muscle weakness in hip girdle and thigh muscles Absent/reduced tendon reflexes Dilated, poorly reactive pupils
371
List the investigations in LEMS
Auto-antibody serology - serum P/Q-type VGCC antibodies +ve NCS * Typically low initial CMAP * Decremental responses to low-frequency repetitive nerve stimulation
372
List the treatment approaches to LEMS
Treat malignancy Symptomatic * Amifampridine * Pyridostigmine
373
Give the hall mark in Prion diseases
Progressive dementia and motor dysfunction
374
List 3 types of prion diseases
Sporadic Creutzfeldt-Jakob disease (sCJD) Genetic prion diseases * Familial CJD * Gerstmann-Straussler-Scheinker * Fatal familial insomnia Acquired prion diseases * Iatrogenic CJD * Variant CJD
375
List the investigations in prion diseases
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
List the common metastatic brain tumours
Lung Breast Melanoma Kidney Stomach Prostate Thyroid
377
List the primary malignant tumours of neuroepithelial tissue
Astrocytoma Oligodendroglioma Oligoastrocytoma Ependymoma Lymphoma Medulloblastoma
377
List the benign brain tumours
Meningioma Neurofibroma
378
List the etiological risk factors for glioma
Ionising radiation Genetic syndromes * Neurofibromatosis type 1 * Tuberous sclerosis complex * Li-Fraumeni syndrome * Turcot syndrome
379
List the investigations and findings for meningioma
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
List the meningitis causative organisms by age group
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
Where does meningioma arise from
Meningothelial cells of the arachnoid layer (arachnoid-cap cells)
382
Compare CSF features of bacterial vs viral meningitis
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
Give the meningococcal disease antibiotic prophylaxis
oral ciprofloxacin single dose
384
List the symptoms for meningitis
Headache Neck stiffness Photophobia Fever Altered consciousness Rash Seizures Shock
385
Describe Kernig’s and Brudzinski’s sign
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
Give the first line investigation in meningitis
Blood culture
387
List the serum electrolyte features in meningitis
Acidosis Hypokalaemia Hypocalcaemia Hypomagnesaemia Low sodium (TB meningitis)
388
List the contraindications for lumbar puncture
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
Give the antibiotics in meningitis
IM/IV benzylpenicillin (children, adults) IV ceftriaxone/cefotaxime (adults)
390
List the causes of encephalitis
(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
Give the signs and symptoms in encephalitis
Acute/subacute onset of a febrile illness Altered mental status Focal neurological abnormalities Seizures
392
Give the diagnostic criteria for encephalitis
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
Give the empirical treatment for encephalitis
Immunocompetent - Aciclovir Immunocompromised - Aciclovir AND ganciclovir AND foscarnet
394
List the symptoms and signs in brain abscess
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
List the most common aetiology for brain abscess by age
Neonates - Proteus mirabilis and Citrobacter species Children - Streptococcus species in combination with cyanotic heart disease Adults - Streptococcus and Staphylococcus species
396
Give the antibiotic of choice in brain abscess
Vancomycin + Metronidazole/clindamycin + third generation cephalosporin (ceftriaxone, cefotaxime)
397
Give the neuroimaging sign in brain abscess
1 or more ring-enhancing lesions
398
Give the triad in normal pressure hydrocephalus
Clinical features of hydrocephalus without significantly elevated CSF * levodopa-unresponsive gait apraxia * urinary incontinence * cognitive impairment
399
List the cardinal features of levodopa-unresponsive gait apraxia
A slow, cautious gait Gait initiation failure Unsteadiness Reduced stride length Shuffling gait Falls Freezing
400
How much CSF is produced by the choroid plexus and is reabsorbed at the arachnoid granulations every minute.
0.5 mL
401
List the investigations for normal pressure hydrocephalus
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
Give the management for normal pressure hydrocephalus
Ventriculoperitoneal shunt surgery
403
List the complications of ventriculoperitoneal shunt surgery
subdural haematoma mechanical obstruction infection
404
What features of migraine is more common in children?
Nausea, vomiting and abdominal pain
405
What are the first-line treatments for spasticity in multiple sclerosis
Baclofen and gabapentin
406
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
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
What is a contraindication to triptan use
Cardiovascular disease
408
List the adverse effects of Lamotrigine
Stevens-Johnson syndrome and toxic epidermal necrolysis Drug reaction with eosinophilia and systemic symptoms (DRESS)
409
410
Give the presentation of Stevens-Johnson syndrome after lamotrigine
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
When is carotid endarterectomy considered for TIA
carotid artery stenosis >50% (NASCET criteria) on the side contralateral to the symptoms
412
What does DVLA say about epilepsy
The person with epilepsy may qualify for a driving licence if they have been free from any seizure for 1 year.
413
What drug is used to prevent vasospasm in aneurysmal subarachnoid haemorrhages
Nimodipine
414
What is Ondansetron selective for
5-HT1 antagonist
415
What is the first line management in pituitary apoplexy
IV hydrocortisone
416
List the order of drugs to give in status epilepticus
1. Buccal midazolam/IV lorazepam 2. IV lorazepam 3. IV phenytoin/levetiracetam/sodium valproate 4. Rapid sequence induction of anaesthesia using thiopental sodium
417
What can be used to differentiate a general tonic-clonic/partial seizure from a non-epileptic pseudo seizure
Elevated serum prolactin 10 to 20 minutes after an episode
418
Give the first line treatments for neuropathic pain
amitriptyline, duloxetine, gabapentin, pregabalin
419
List the causes for neuropathic pain
diabetic neuropathy post-herpetic neuralgia trigeminal neuralgia prolapsed intervertebral disc
420