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Alex's MRCP Cards > Neurology > Flashcards

Neurology Flashcards

1
Q

Frontal lobe abnormalities?

A
  • Difficulties with task sequencing
  • Difficulties with executive skills
  • Expressive aphasia (Broca’s) in the inferior frontal gyrus
  • Anosmia
  • Primitive reflexes
  • Perseveration (repeatedly asking same question or doing same task)
  • Changes in personality
  • Inability to generate a list
  • Disinhibition
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2
Q

Parietal lobe abnormalities?

A
  • Apraxias: loss of the ability to execute learned purposeful movements
  • Neglect
  • Astereognosis (unable to recognise object by feeling) = tactile agnosia
  • Homonymous inferior quadrantanopia
  • Sensory inattention
  • Acalculia: inability to perform mental arithmetic
  • Gerstmann’s syndrome (lesion of dominant parietal):
    • Alexia: in ability to read
    • Acalculia
    • Finger agnosia
    • Right-left disorientation.
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3
Q

Temporal lobe abnormalities?

A
  • Homonymous superior quadrantanopia
  • Prosopagnosia (difficulty recognising faces)
  • Wernike’s (recepTive) aphasia
  • Memory impairment
  • Auditory agnosia
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4
Q

Occipital lobe abnormalities?

A
  • Cortical blindness (blindness due to damage to visual cortex, may present as Anton syndrome: there is blindness but patient is unaware or denies blindness)
  • Homonymous hemianopia
  • Visual agnosia (seeing but not percieving objects - it is different to neglect since in agnosia the objects are seen and followed but cannot be named)
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5
Q

Spinal tract dysfunction?

A
  1. Dorsal column dysfunction: (joint position and light touch)
  2. Spinothalamic dysfunction: (pinprick and temperature)
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6
Q

Mnemonic for homonomous quadrantanopia?

A

PITS

Parietal = inferior, Temporal = superior

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7
Q

Upper and lower bitemporal hemianopia?

A

Optic Chiasm

  • Upper > Lower = inferior compression - pituitary tumour
  • Lower > Upper = superior compression - craniopharyngioma
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8
Q

Causes of nystagmus?

A
  • Visual disturbances
  • Lesions of the labyrinth
  • The central vestibular connections
  • Brain stem or cerebellar lesions.
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9
Q

Causes of SAH?

A
  • 85% are due to rupture of berry aneurysms
    • Associated with APKD, Ehlers-Danlos syndrome and coarctation of the aorta
  • AV malformations.
  • Trauma
  • Tumours
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10
Q

ECG changes in SAH?

A
  • Deep symmetrical T wave Inversion
  • Prolonged QT interval
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11
Q

Features of specific intracranil venous thromboses?

A

Sagittal

  • May present with seizures and hemiplegia
  • Parasagittal biparietal or bifrontal hemorrhagic infarctions are sometimes seen

Cavernous

  • Other causes of cavernous sinus syndrome: local infection (e.g. Sinusitis), neoplasia, trauma
  • Ophthalmoplegia due to IIIrd, IVth and VIth nerve damage
  • Trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
  • Central retinal vein thrombosis
  • Swollen eyelids

Lateral

  • VIth and VIIth cranial nerve palsies
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12
Q

Features of Wernicke’s

A
  • Nystagmus
  • Ophthalmoplegia
  • Ataxia
  • Confusion, altered GCS
  • Peripheral sensory neuropathy
  • Impairment of short-term memory
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13
Q

Triad of normal pressure hydrocephalus?

A
  • Urinary incontinence
  • Dementia and bradyphrenia (slowness of thought)
  • Gait abnormality (may be similar to parkinson’s disease)

Cause = reduced CSF absorption by arachnoid villi

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14
Q

Features, risk factors, investigations, management of Idiopathic Intracranial HTN (BIH)?

A

Features

  • Headache
  • Blurred vision
  • Papilledema (usually present)
  • Enlarged blind spot
  • Sixth nerve palsy may be present

Risk Factors

  • Obesity
  • Female sex
  • Pregnancy
  • Drugs: oral contraceptive pill, steroids, tetracycline, vitamin A

Ix

  1. CT Scan
  2. LP
  3. Cerebral MRI with MR Venography

Mx

  • Weight loss
  • Diuretics e.g. Acetazolamide
  • Steroids
  • Repeated lumbar puncture
  • Surgery: optic nerve sheath decompression and fenestration may be needed to prevent optic nerve damage. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
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15
Q

Criteria for carotid endarterectomy?

A
  • Recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled
  • Should only be considered if carotid stenosis > 70% according ECST criteria or > 50% according to NASCET criteria
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16
Q

Stroke by anatomy?

A

Anterior Cerebral Artery

  • Contralateral hemiparesis and sensory loss, lower extremity > upper
  • Disconnection syndrome (akinetic mute patient)

Middle Cerebral Artery

  • Contralateral hemiparesis and sensory loss, upper extremity > lower
  • Contralateral hemianopia
  • Aphasia (Wernicke’s)
  • Gaze abnormalities

Posterior Cerebral Artery

  • Contralateral hemianopia with macular sparing
  • Disconnection syndrome
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17
Q

Atypical strokes?

A

Lacunar

  • Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia

Lateral Medulla (Posterior inferior CA - Wallenberg’s syndrome)

  • Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy
  • Contralateral: limb sensory loss

Pontine

  • VI nerve: horizontal gaze palsy
  • VII nerve
  • Contralateral hemiparesis

Basilar Artery

  • Most of patients present with nausea, vertigo and vomiting
  • Some present with motor deficits, dysarthria and speech involvement or headaches
  • May present with visual disturbances. This includes abducens nerve palsy, conjugate gaze palsy,
    internuclear ophthalmoplegia and ocular bobbing
  • Locked-In Syndrome: patient is awake but is unable to respond in anyway except by vertical
    gaze and blinking (lesion is in ventral pons)
  • 70% of patients presenting with basilar artery territory stroke are hypertensive.
  • Management includes vigorous control of hypertension and antiplatelet agents.
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18
Q

Bamford Stroke Classification?

A
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19
Q

Spinal Cord Syndromes

A
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20
Q

Syringomyelia - what is it? Features?

A

Developmental, slowly enlarging cavitary expansion (longitudinal) of the cervical cord that produce progressive myelopathy

Associated with chiari malformation

Features

  • Maybe asymmetrical initially
  • Slowly progressives, possibly over years
  • Motor: wasting and weakness of arms
  • Sensory: spinothalamic sensory loss (pain and temperature)
  • Loss of reflexes, bilateral upgoing plantars
  • Also seen: horner’s syndrome
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21
Q

Subclavian steal syndrome?

A

Retrograde flow in the vertebral artery due to proximal subclavian artery stenosis. Neurological symptoms are precipitated by vigorous exercise with the arm above the head, such as painting a wall.

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22
Q

Subacute combined degeneration of the spinal cord? Features? Causes?

A

Degeneration of the posterior and lateral columns of the spinal cord as a result of vitamin B12 deficiency (most common), vitamin E deficiency or Friedrich’s ataxia. It is usually associated with pernicious anemia.

  • Patchy losses of myelin in the dorsal and lateral columns.
  • Present with progressive weakness of legs, arms, trunk,
    tingling and numbness.
  • Visual & Mental changes may also be present.
  • Bilateral spastic paresis may develop and pressure, vibration
    and touch sense are diminished.
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23
Q

Von Hippel-Lindau?

A

Autosomal Dominant - chromosome 3

Retinal and cerebellar haemangiomas

  • Cerebellar hemangiomas (Can secrete crythyropiotiene that causes secondary polycythemia)
  • Retinal hemangioma: vitreous hemorrhage
  • Renal cysts (premalignant)
  • Pheochromocytoma
  • Extra-renal cysts: epididymal, pancreatic,hepatic
  • Endolymphatic sac tumours
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24
Q

Freidreich’s Ataxia?

A

Autosomal Recessive

Trinucelotide repeat disorder - GAA repeat, X25 gene, chromosome 9

Onset = 10-15 yrs

Neuro Features

  • Absent ankle jerks/extensor plantars
  • Cerebellar ataxia
  • Optic atrophy
  • Spinocerebellar tract degeneration

Other Features

  • Hypertrophic obstructive cardiomyopathy (90%, most common cause of death)
  • Diabetes mellitus (10-20%)
  • High-arched palate
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25
Q

Tuberous Sclerosis?

A

Autosomal Dominant

Cigarettes and coffee with a rough stupid person with a butterfly on his nose while he is dancing

Cutaneous Features

  • Depigmented ‘ash-leaf’ spots which fluoresce under UV light
  • Roughened patches of skin over lumbar spine (Shagreen patches)
  • Adenoma sebaceum: butterfly distribution over nose
  • Fibromata beneath nails (subungual fibromata)
  • Café-au-lait spots may be seen

Neurological Features

  • Developmental delay
  • Epilepsy (infantile spasms or partial)
  • Intellectual impairment

Other Features

  • Retinal hamartomas: dense white areas on retina (phakomata)
  • Rhabdomyomas of the heart
  • Gliomatous changes can occur in the brain lesions
  • Polycystic kidneys, renal angiomyolipomata
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26
Q

Neurofibromatosis general details?

A

Autosomal Dominant

NF1

  • Chromosome 17 (17 characters in NF)

NF2

  • Chromosome 22 (all the 2s)
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27
Q

Neurofibromatosis features?

A

NF1

  • Café-au-lait spots (= 6, 15 mm in diameter)
  • Axillary/groin freckles
  • Peripheral neurofibromas
  • Iris: Lisch nodules in > 90%
  • Scoliosis

NF2

  • Bilateral acoustic neuromas
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28
Q

Hereditary Sensorimotor Neuropathy (Charcot-Marie-Tooth Disease)?

A

Autosomal Dominant

  • Defect in PMP-22 gene - codes for myelin
  • Onset - puberty
  • Motor symptoms predominate
  • Distal muscle wasting, pes cavus (high arched), clawed toes
  • Foot drop, leg weakness often first features
  • Nerve Conduction Velocity is greatly reduced <30m/second
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29
Q

MND Patterns?

A

Amyotrophic Lateral Sclerosis

  • Typically LMN signs in arms and UMN signs in legs

Primary Lateral Sclerosis

  • UMN signs only

Progressive Muscular Atrophy

  • LMN signs only
  • Affects distal muscles before proximal
  • Carries best prognosis

Bulbar Palsy

  • Palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function
    of brainstem motor nuclei
  • Carries worst prognosis
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30
Q

Features of MND?

A
  • Fasciculation
  • Absence of sensory signs/symptoms
  • LMN signs in arms and UMN signs in legs
  • Wasting of the small hand muscles/tibialis anterior is common
  • Doesn’t affect external ocular muscles
  • No cerebellar signs
  • Abdominal reflexes usually preserved
31
Q

Lesions producting both UMN and LMN signs?

A
  1. Subacute combined degeneration of the cord
  2. Motor neuron disease
  3. Friedreich’s ataxia
  4. Syringomyelia
  5. Syringobulbia
  6. Taboparesis (syphilis)
  7. Conus medullaris lesion
32
Q

Drugs for generalised vs partial seizures?

A

Generalised = sodium valproate –> lamotrigine, carbamezapine

Partial = carbamezapine –> lamotrigine, sodium valproate, gabapentin

33
Q

Absence seizures?

A

Mostly seen in kids

3-10 years, girls 2x more than boys

Features

  • Absences last a few seconds and are associated with a quick recovery
  • Seizures may be provoked by hyperventilation or stress
  • The child is usually unaware of the seizure
  • They may occur many times a day
  • EEG: bilateral, symmetrical 3Hz (spike and wave) pattern

Management

  • Sodium valproate and ethosuximide are first-line treatment
  • Good prognosis - 90-95% become seizure free in adolescence
34
Q

Stopping AEDs?

A

AED cessation can be considered if seizure free for > 2 years – Stop AEDs over 2-3 months

35
Q

AEDs in pregnancy?

A
  • Sodium valproate: associated with neural tube defects
  • Phenytoin: associated with cleft palate - need VIT K in last month of pregnancy
  • Lamotrigine: studies to date suggest the rate of congenital malformations may be low. The dose of lamotrigine may need to be increased in pregnancy
  • Carbamazepine: often considered the least teratogenic of the older antiepileptics

Breast feeding considered safe

36
Q
A
37
Q

Seizure features suggestive of NEAD?

A
  • Asynchronous limb movements
  • Undulating motor activity
  • Purposeful movements
  • Rhythmic pelvic movements
  • Side-to-side head shaking
  • Biting the tip of the tongue (as opposed to the side)
  • Ictal crying
  • Vocalisation during the ‘tonic–clonic’ phase
  • Closed eyelids, resistance to eyelid opening
  • Lack of cyanosis and rapid post-ictal reorientation
38
Q

Frequency of tremor in PD?

A

3-5 Hz

39
Q

Differences between drug induced parkinsonism and PD? Causes of DIP?

A

In DIP…

  • Motor symptoms are generally rapid onset and bilateral
  • Rigidity and rest tremor are uncommon

Causes

  • Phenothiazines: e.g. Chlorpromazine
  • Butyrophenones: haloperidol, droperidol
  • Metoclopramide
40
Q

PD Drugs?

A

Dopamine Receptor Agonists (>75 yrs)

  • Bromocriptine, Pramipexole, Ropinirole, Cabergoline, Apomorphine
  • Associated with fibrosis (pulm, retroperitoneal, cardiac) - Ropinirole least so
  • Can cause impulse control disorders and excessive daytime somnolence

L-Dopa (<75 yrs)

  • Combined with decarboxylase inhibitor (prevents peipheral metabolism)
  • Decreased effectiveness over time

MAO-B Inhibitors

  • Selegiline
  • Inhibit breakdown of dopamine

Amantadine

  • Increases dopamine release and inhibits uptake at synapses

COMT Inhibitors

  • Entacapone
  • COMT is an enzyme involved in dopamine breakdown - used as an adjunct in levodopa therapy
  • Used in established PD
41
Q

Multiple system atrophy?

A

Features

  • Parkinsonism
  • Autonomic disturbance (atonic bladder, postural hypotension)
  • Cerebellar signs

Example = Shy-Drager syndrome

42
Q

Progressive supranuclear palsy?

A

Parkinsonism, impairment of vertical gaze

  • Gradual deterioration and death of selected areas of the brain
  • Features
    • Impairment of vertical gaze
    • Parkinsonism
    • Falls
    • Slurring of speech
    • Cognitive impairment

May complain of difficulty reading or descending stairs

43
Q

CJD Features?

A
  • Rapidly progressive, severe and invariably fatal (usually within few months)
  • Dementia
  • Cerebellar ataxia
  • Defuse myoclonic jerks
  • Other neurological abnormalities.
44
Q

Investigation results in CJD?

A
  • The EEG patern is characteristic (diffuse non specific slowing periodic sharp wave complexes- PSWCs of 1 – 2 Hz), but diagnosis relies on either espiecalized tests for prion protein in CSF or direct brain biopsy.
  • Pulvinar Sign on cranial MRI > 90% pathological in vCJD (Not Sporadic)
  • Prion protien in tonsils
  • 14-3-3 protien in CSF
45
Q

Hemiballism?

A
  • Involuntary, sudden, jerking movements which occur contralateral to the side of the lesion
  • Primarily affect the proximal limb musculature whilst the distal muscles may display more choreiform-like movements.
  • Symptoms may decrease during sleeping.
  • Etiology: stroke in elders, infection or inflammatory in young.
  • Antidopaminergic agents (e.g. Haloperidol) are the mainstay of treatment. Tetrabenazine may be considered when long-term therapy is required.
46
Q

Causes of Chorea?

A
  • Huntington’s disease, Wilson’s disease, ataxic telangiectasia
  • SLE, anti-phospholipid syndrome
  • Rheumatic fever: Sydenham’s chorea
  • Drugs: oral contraceptive pill, L-dopa, antipsychotics
  • Chorea gravidarum
  • Thyrotoxicosis
  • Polycythemia rubra vera
  • Carbon monoxide poisoning
  • Neuroacanthocytosis
  • Cerebrovascular disease
47
Q

Types of MS?

A

Relapsing-remitting

  • Characterized by unpredictable relapses followed by periods of months to years of relative quiet (remission) with no new signs of disease activity.
  • 85–90% of individuals with MS.

Secondary progressive

  • Initial relapsing-remitting MS, then begin to have progressive neurologic decline between acute attacks without any definite periods of remission.
  • Median time between disease onset and conversion from relapsing-remitting to secondary progressive MS is 19 years.

Primary progressive

  • 10–15%
  • Never have remission after their initial MS symptoms. It is characterized by progression of disability from onset, with no, or only occasional and minor, remissions and improvements.
  • Age of onset for the primary progressive subtype is later than other subtypes.

Progressive relapsing

  • Describes those individuals who, from onset, have a steady neurologic decline but also suffer clear superimposed attacks. This is the least common of all subtypes.
48
Q

Features of MS?

A

Visual

  • Optic neuritis: common presenting feature
  • Optic atrophy
  • Uhthoff’s phenomenon: worsening of vision following rise in body temperature (hot bath)
  • Internuclear ophthalmoplegia

Sensory

  • Numbness
  • Trigeminal neuralgia
  • Lhermitte’s syndrome: paraesthesiae in
    limbs on neck flexion

Motor

  • Spastic weakness

Cerebellar

  • Ataxia, Tremor

Others

  • Urinary incontinence
  • Sexual dysfunction
  • Intellectual deterioration
49
Q

Good prognosis features in MS?

A
  • Female sex
  • Young age of onset
  • Relapsing-remitting disease
  • Sensory symptoms
  • long interval between first two relapses

Typical patient carries better prognosis than atypical presentation

50
Q

Investigations in MS?

A

Diagnosis = demonstration of lesions dissemintated in time and space

MRI

  • High signal T2 lesions
  • Periventricular plaques

CSF

  • Oligoclonal bands (and not in serum)
  • Increased intrathecal synthesis of IgG

Visual evoked potentials

  • Delayed, but well preserved wave form
51
Q

Criteria for beta interferon in MS? Other drugs?

A
  • Relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
  • Secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)

Reduces number of relapses and MRI changes.
However doesn’t reduce overall disability

  • *Glatiramer acetate** - immunomodulating drug
  • *Natalizumab** - a recombinant monoclonal antibody that antagonises a4b1-integrin found on the surface of leucocytes, thus inhibiting migration of leucocytes across the endothelium into parenchymal tissue
52
Q
A
53
Q

Argyll-Robertson pupil?

A
  • small irregular pupils that do not react to light but react to accommodation
  • Whore’s eye - associated with tertiary syphilis
  • “Accommodate but do not react”

Other causes = MS, Sarcoidosis, DM

54
Q

Location of lesion in Horner’s syndrome from location of anhydrosis?

(STC)

A
55
Q

Gaze palsies?

A
56
Q

Surgical third nerve palsy?

A
  • Down and out
  • Ptosis
  • Pupil dilated (posterior communicating artery aneurysm) - can be PAINFUL
57
Q

Weber’s syndrome?

A

ipsilateral third nerve palsy with contralateral hemiplegia - caused by midbrain strokes (cerebral peduncle)

58
Q

Investigations in Myasthenia Gravis?

A

Tensilon test: IV edrophonium reduced muscle weakness temporarily
CT thorax to exclude thymoma
CK normal

59
Q

Drugs that exacerbate myasthenia?

A
  • Beta-blockers (theoretical worsening based on propensity to cause side effects of fatigue and weakness)
  • Gentamicin, Aminoglycosides and Tetracycline
  • Lithium
  • Magnesium
  • Penicillamine
  • Phenytoin
  • Quinidine, procainamide, verapamil, contrast agents.
  • Chloroquine
  • Prednisolone
60
Q

Paraneoplastic syndromes affecting nervous system?

A

Lambert-Eaton myasthenic syndrome

  • Associated with small cell lung cancer (also breast and ovarian)
  • Antibody directed against pre-synaptic voltage gated calcium channel in PNS
  • Can also occur independently as autoimmune disorder
  • Increased muscle strength followed by weakness eventually.

Anti-Hu (imagine H sticks as 2 lungs or 2 brain hemispheres)

  • Associated with small cell lung carcinoma and neuroblastomas
  • Sensory neuropathy - may be painful
  • Cerebellar syndrome
  • Encephalomyelitis

Anti-Yo (imagine Y as lady’s private organ)

  • Associated with ovarian and breast cancer
  • Cerebellar syndrome

Anti-GAD antibody

  • Associated with breast, colorectal and small cell lung carcinoma
  • Stiff person’s syndrome or diffuse hypertonia

Anti-Ri

  • Associated with breast and small cell lung carcinoma
  • Ocular opsoclonus-myoclonus
61
Q

Peripheral Neuropathy - axonal vs demyelination?

A
62
Q

Peripheral neuropathy - sensory vs motor?

A

Nerve conduction studies

  • Demyelination - Reduced conduction velocity, normal amplitude
  • Axonal - Normal conduction velocity, reduced amplitude
63
Q
A
64
Q

Drugs causing peripheral neuropathy?

A
  • Antibiotics: nitrofurantoin, metronidazole
  • Amiodarone
  • Isoniazid
  • Vincristine and most of the anti-cancer chemotherapy
  • Tricyclic antidepressants
65
Q

Features of HSV Encephalitis? Pathophysiology? Investigation?

A

Features

  • Fever, headache, psychiatric symptoms, seizures,
    vomiting
  • Focal features e.g. Aphasia
  • Peripheral lesions (e.g. Cold sores) have no relation
    to presence of HSV encephalitis

Pathophysiology

  • HSV-1 responsible for 95% of cases in adults
  • Typically affects temporal and inferior frontal lobes

Investigation

  • CSF: lymphocytosis, elevated protein
  • PCR for HSV
  • CT: medial temporal and inferior frontal changes (e.g. Petechial hemorrhages) - normal in one-third of patients
  • MRI is better
  • EEG pattern: lateralised periodic discharges (2 Hz)
66
Q

Sub-acute sclerosing panencephalitis?

A

Result of chronic measles infection

Features

  • Initially: decline in proficiency in school.
  • Followed by diffuse myoclonic jerks in association with focal and generalised seizures and visual deterioration due to choiroidoretinitis.
  • Followed by pyramidal signs, rigidity and progressive unresponsiveness.
  • Finally the patient lies decorticated followed by death.
67
Q

HIV neurocomplications? (Generalised neurological disease)

A
  1. Encephalitis
    • May be due to CMV or HIV itself
    • HSV encephalitis but is relatively rare in the context of HIV
    • CT: edematous brain
  2. Cryptococcus
    • Headache, fever, malaise, nausea/vomiting, seizures, focal
      neurological deficit
    • CSF: high opening pressure, India ink test positive
    • CT: meningeal enhancement, cerebral edema
    • Meningitis is typical presentation but may occasionally cause a space occupying lesion
  3. Progressive multifocal leukoencephalopathy (PML)
    • Widespread demyelination
    • Due to infection of oligodendrocytes by human papovirus (jc virus)
    • Symptoms, subacute onset : behavioural changes, speech, motor, visual impairment
    • CT: single or multiple lesions, no mass effect, don’t usually
      enhance, Low attenuation diffusely
    • MRI is better - high-signal demyelinating white matter lesions are seen in advanced HIV.
  4. AIDS Dementia Complex
    • Symptoms: behavioural changes, motor impairment
    • CT: cortical and subcortical atrophy
68
Q

HIV neurocomplications? (Focal neurological lesions)

A
  1. Toxoplasmosis
    • Constitutional symptoms, headache, confusion, drowsiness
    • CT: usually single or multiple ring enhancing lesions, mass
      effect may be seen
    • Management: sulfadiazine and pyrimethamine
  2. Primary CNS Lymphoma
    • Associated with the Epstein-Barr virus
    • CT: single or multiple ring enhancing lesions
  3. Tuberculosis
    • Much less common
    • CT: Single enhancing lesion
69
Q

Myotonic Dystrophy?

A
  • Inherited myopathy - develops at around 20-30 yrs
  • Affects skeletal, cardiac and smooth muscle
  • Autosomal Dominant
  • Trinucleotide repeat disorder

DM1

  • DMPK gene on chromosome 19
  • Distal weakness more prominent

DM2

  • ZNF9 gene on chromosome 3
  • Proximal weakness more prominent
70
Q

Features of myotonic dystrophy?

A

General

  • Myotonic facies (long, ‘haggard’ appearance)
  • Frontal balding
  • Bilateral ptosis
  • Cataracts
  • Dysarthria

Other Features

  • Myotonia (tonic spasm of muscle)
  • Weakness of arms and legs (distal initially)
  • Mild mental impairment
  • Diabetes mellitus
  • Testicular atrophy
  • Cardiac involvement: heart block, cardiomyopathy
  • Dysphagia
71
Q

Management of cluster headache?

A
  • Acute: 100% oxygen, subcutaneous sumatriptan (5-HT1D receptor agonist), nasal lidocaine
  • Prophylaxis: verapamil, prednisolone
  • Consider specialist referral
72
Q

Normal CSF values?

A
  • *Pressure** = 60-150 mm (patient recumbent)
  • *Protein** = 0.2-0.4 g/l
  • HIGH protein = TB, fungal, bacterial meningitis; viral encephalitis; Guillain Barre syndrome, Spinal block (Froin’s syndrome?
  • *Glucose** = > 2/3 blood glucose
  • *Cells**: red cells = 0, white cells < 5/mm³
  • HIGH lymphocytes = viral meningitis/encephalitis, TB meningitis, partially treated bacterial meningitis, Lyme disease, Bechet’s, SLE, lymphoma, leukaemia
73
Q

Features of post-LP headache? Factors which contribute?

A
  • Usually develops within 24-48 hours following LP but may occur up to one week later
  • May last several days
  • Worsens with upright position
  • Improves with recumbent position

Management

  • Supportive initially (analgesia, rest)
    If pain continues for more than 72 hours then specific treatment is indicated, to prevent subdural hematoma
  • Blood patch, epidural saline, intravenous caffeine

Alex's MRCP Cards (13 decks)

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