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Neurology Flashcards

1
Q

Parkinson’s disease definition

A

Neurodegenerative disease caused by the disruption of dopaminergic neurotransmission in the basal ganglia. Histological loss of melanin containing dopaminergic neurones in the substantia nigra and cytoplasmic inclusions known as lewy bodiers in surviving neurones. 60-80% neurone loss before clinical symptoms.

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2
Q

Dementia in parkinsons disease

A

Late, 15-30% patients. Earlier occurance of cognitive symptoms (i.e. within 1 year of motor symptoms may suggest lewy body dementia)

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3
Q

Parkinson’s vs Parkinsonism

A

Parkinson’s asymmetrical distribution of signs, good reponse to levodopa, absent parkinsonian plus signs, progressive progression.
Parkinsonism more symmetrical, poor response to levodopa, may have addditional signs to suggest PP syndromes

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4
Q

Parkinsonian plus syndromes

A

MSA
PSP
CBD

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5
Q

MSA

A

Parkinsonism, autonomic failure, cerebellar dysfunction and pyramidal signs.
Progressive loss of neuronal/oligodendronal cells at numerous sites in CNS, with relative sparing of globus pallidus, caudate nucleus, CST and anterior horn cells.

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6
Q

PSP

A

Most common PP+. Multiple neurotransmitter pathways (cholinergic, adrenergic, dopaminergic).
Abnormal vertical then horizontal saccades. Difficulty opening eyes, early and prominent falls, speach/swallow, frontal symptoms of depression, apathy, cognitive impairment.
Symmetrical parkinsonian features.

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7
Q

CBD

A 
Frontoparietal cortical atrophy + extrapyramidal degeneration. 
Limb aprexia (&alien limb syndrome) + cortical sensory loss.
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8
Q

What is parkinsonism?

A

Movement disorder characterised by bradykinesia and at least one of rigidity, tremor or postural instability

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9
Q

Carpel tunnel syndrome

A

Look for: weakness of flexion, abduction and opposition of thumb. Decreased sensation over lateral three and a half fingers. Tinel’s sign (tingling in median nerve distribution on percussion of median nerve). Phalen’s sign (hyperextension of wrist for 1 minute reproduces symptoms. Look for a scar of previous median nerve decompression.
Associations: Acromegaly, myxoedema, rheumatoid arthritis, occupational trauma, pregnancy.

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10
Q

Chorea

A

Sydenham’s chorea, Huntington’s disease, polycythemia vera, chorea gravidarum, drug induced, systemic disease (SLE, thyrotoxicosis, etc). If hemichorea, consider infarction or tumour.

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11
Q

Ankylosing spondylitis

A

Features shown: ‘Question mark’ posture due to loss of lumbar lordosis, fixed kyphoscoliosis of thoracic spine and hyperextension at cervical spine and some protuberance of the abdomen.
Look for: whole body turning when patient tries to rotate neck, inability of the occiput to make contact with the wall when the heels and back are against the wall (occiput-to-wall distance), limited spinal movement (increased finger floor distance and Schober’s test), reduced chest expansion, eyes (iritis and anterior uveitis), aortic regurgitation and apical lung fibrosis.

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12
Q

Homonymous hemianopia

A

Lesion behind the optic chiasm.

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13
Q

Bitemporal hemianopia

A

Lesion at the optic chiasm
DDx pituitary tumour, craniopharyngioma, suprasellar meningioma, glioma, metastasis
Pituitary tumours compress from below (upper temporal first), craniopharyngiomas compress from above (lowe temporal field first)
Look for: acromegaly, cushings, hypopituitarism, gynaecomastia, sarcoid, tuberculosis, malignancy

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14
Q

Homonymous upper quadrantopia

A

Temporal cortex

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15
Q

Homonymous lower quadranopia

A

Parietal cortex

PITS

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16
Q

What do you understand by homonymous

A

Identical pattern of visual field defects in each eye

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17
Q

Kennedy-Foster syndrome

A

Ipsilateral optic atrophy 2* to compression of optic nerve

Contralateral paplilloedema secondary to raised ICP

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18
Q

Myotonic Dystrophy Examination

A

Face - myopathic pacies, thin expressionless, wasting of facial and SCN muscles, bilateral ptosis, frontal balding, dysarthria from myotonia of tongue and pharynx
Hands - myotonia (grip my hand, not let go), wasting and weakness distally with areflexia
Percussion myotonia - percus thenar eminence and watch for involuntary thumb movement
Additional - catracts, CM, PPM from brady/tachy arrythmias, diabetes, testicular atrophy, dysphagea

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19
Q

Myotonic dystrophy genetics

A

AD, with genetic anticipation
DM1 - CTG trinucleotide repeat DMPK gene Chr19
DM2 - CCTG trinucleotide repeat within ZNF9 gene on chr 3
DM1 in 20s and 30s, DM2 later (but variable)

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20
Q

Diagnosing myotonic dystrophy

A

Clinical examination
EMG - dive bomber potentials
Genetic testing

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21
Q

Management of myotonic dystrophy

A

Respiratory and cardiac complications leading causes of mortality
Weakness - no treatment
Phenytoin may help myotonia
High risk of complications from anaesthesia

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22
Q

DDx ptosis

A

Bilateral - MG, myotonic dystrophy, congenital

Unilateral - 3rd nerve palsy, horners syndrome

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23
Q

Interpreting cerebellar lesion

A

Ipsilateral cerebellar signs in the limbs

Nystagmus - maximal fast paced direction towards (when looking at) the lesions

But** in vestibular/VIII lesions maximum away from the lesion

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24
Q

Causes of cerebellar syndrome

A 
PASTRIES
Paraneoplastic 
Alcoholic 
Sclerosis (MS)
Tumour
Rare (Freidrich, ataxia telangectasia)
Iatrogenic (phenytoin)
Endocrine (hypothyroidism)
Stroke
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25
Q

Investigating MS

A

GCS - oligoclonal bands
MRI - periventricular white matter changes
Visual Evoked Potentials - dleayed velocity but normal amplitude to suggest optic neuritis

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26
Q

MS treatment

A

MDT - nurses, PT, OT, social worker, physician
Treatments:
INF-b reduces relapse rate but does not affect progression.
mAb - natalizumab (anti a4 integrin, blocks T cell trafficking) and alemtuzumab (anti-CD-52, lymphocyte depletion)
Symptomatic - methylprednisolone will shorten duration of attack
Anti-spasmodics like baclofen
Neuropathic pain - carbamazepine
Bladder and bowel regimes

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27
Q

Pyramidal weakness

A

Extensors weaker than flexors in upper limbs

Flexors weaker than extensore in lower limbs

28
Q

Define stroke and TIA

A

Stroke - rapid onset focal neurological deficit secondary to vascular lesion lasting >24 hours
TIA - rapid onset focal neurological deficit secondary to vascular lesion lasting <24 hours

29
Q

Bamford classification of stroke

A

TACS - HHH (hemianopia, higher dysfunction, hemiplegia)
PACS - 2/3 TACS
LACS - pure hemi motor or sensory loss, ataxic hemiplegia
POCS -
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

30
Q

Lateral Medullary Syndrome (Wallenberg)

A

PICA occlusion
Ipsilateral cerebellar, horner, palatal paralysis, loss of V sensation
Contralateral loss of pain and temperature sensation

31
Q

Subacute combined degeneration of the cord

A

Absent reflexes with upgoing plantars

32
Q

Spastic legs - examination

A

Observation - wheelchair, sticks, disuse atrophy and contractures
Increased tone, ankle clonus
Weakness
Hyperreflexia and extensor plantats
Scissoring gait
Other - look at back for surgical scars, syringomyelia (upper limb signs), anterior spinal artery thrombosis, hereditary spastic parapalegia (+ve FH), SCDC, Friedrich ataxia, cord compression

33
Q

Cord compression

A 
Disc prolapse above L2/L1
Malignancy 
Traumatic 
Infection - abscess of TB 
investigation - spinal MRI 
Management - surgical decompression, streroids / Rx for malignant choice
34
Q

Examining syringomyelia

A

Weakness/wasting small musles of hand, areflexia, dissociated sensory loss in upper limbs and chest, loss of pain (STT) but preserved vibration and proprioception (dorsal column)
Scars from burns
Charcot joints
Pyramidal weakness in lower limbs with upgoing plantars
Kyphscoliosis and horners
If syrinx extends into brainstem (syringobulbia) may be cerebellar and lower cranial signs

35
Q

What is syringomyelia

A

Progressively expanding fluid filled cavity (syrinx) within cervical cord, typically spanning several levels
Expands ventrally:
1. STT = pain and loss of temp at level of syrinx
2. Anterior horn cells = segmental LMN weakness at level
3. CST = UMN weakenss below level of syrinx
4. Dorsal columns spared (intact proprioception and vibration sense)
Signs may be asymmetrical
MRI scan

36
Q

What are charcot joints

A 
Painless deformity and destruction of a joint with new bone formation following repeated minor trauma secondary to loss of pain sensation
Tabes dorsalis - hip and knee
Diabetes - foot and ankle
Syringomyelia - elbow and shoulder 
Bisphosphonates can help
37
Q

MND on examination

A 
Inspection: Wasting and fascilculations
Tone: spastic / flaccid
Power: reduced
Reflexes: absent or brisk 
Sensory: normal 
Speech: dysarthria (bulbar - donald duck, nasal, palatal weakness); or pseudobulbar (hot potato, spastic tongue)
Tongue: wasting and fasciculations
No sensory, extra-ocular, cerebellar, or extramyramidal involement
38
Q

MND definition and investigation

A

Progressive neurodgenerative disease of unknown aetiology resulting in axonal degeneration of upper and lower motor neurones. 3 main subtypes:

  1. Amyotrophic Lateral Sclerosis (50%, ALS) - CST predominant = spastic paraparesis or tetraparesis
  2. Progressive muscular atrophy (25%) = Anterior horn cells prdominantly = wasting fasciculations and weakness, best prognosis
  3. Progressive bulbar palsy (25%) = lower cranial nerves and suprabulbar nuclei, speech and swallow problems, worst prognosis
39
Q

MND investigation treatment and prognosticaiton

A

Clinical diagnosis, EMG, MRI brain/spine to r/u cervical cord compression, myelopathy and brainstam lesions
Supportive: PEG feeding and NIPPV
MDT
Rilozule - slow disease progression 3/12 but not affecting function or QoL
Most die within 3 years, usually resp complications
Wost if elderly, female and bulbar onser

40
Q

DDx wasting of hand muscles

A

Anterior horn cell - MND, syringomyelia, cervical cord compression, polio
Brachial plexus - cervical rib, pancoast tumour, trauma
Peripheral nerve - combined medial & ulnar lesions
Muscle - disure atrophy (e.g. RA)

41
Q

What is a fasciculation?

A

Visible muscle twitching at rest
Due to axonal loss results in surviving neurones recruiting and innervaintg more myofibrils than ususal resulting in large motor units
Commonly in MND or syringomyelia

42
Q

Treating parkinsons disease

A

levodopa with peripheral dopa-decarboxylase inhibitor (co-careldopa, co-beneldopa). SE of nausea nad dyskinesia. Effects wear off after few years so best to pick moment. on/off motor fluctuations can be decreases by MR preperations
Dopamine agonists - younger patients, less SE, saves L dopa until necessary. Apomorphine also agonist which can be used as S/C or infusion for pts with severe off periods
MAO-B inhibitors (selegiline) inhibit breakdown of dopamine
Anticholiergics - reduced tremor
COMT inhibitors (e.g. entercapone) - inhibit peripheral breakdown of L dopa thus reducing motor flucutations
Amantadine - increases dopamine release
Surgery / DBS

43
Q

Causes of tremor

A

Resting - PD
Postural - benign essential (50% familial, improves with etoh)
Anxiety, thyrotoxicosis, CO2 and HE, alcohli
intention - cerebellar disease

44
Q

Hereditary sensory motor neuropathy - examination

A

Charcot-Marie-Tooth disease
Wasting distal lower limb muscle with preservation of thigh bulk (inverted champagne appearance), pes cavus, weakness ankle dorsiflexion and toe extension
Variable degree stocking distribution of sensory loss (usuallly mild)
High stepping gait (foot drop) + stamping (loss of proprioception)
Wasting hand muscles
Palpable lateral popliteal nerve

45
Q

Genetics of CMT

A 
Hereditary sensory motor neuropathy 
I (demyelinating)
II (axonal) 
AD - PMP 22 in type 1
Also known as peroneal muscular atrophy
46
Q

Causes of peripheral neuropathy

A

Sensory –> DM, Alcohol, Drugs (isoniazid, vincristine), Vitamin B1 b12
Motor –> Guillain Barre, lead, porphyria, HSMN
Mononeuritis multiplex –> DM, CTD (SLE, RA), vasculitis (PAN, CS), malignancy

47
Q

Friedrich Ataxia - examination

A

Young Adult, wheelchair
Pes cavus
Bilateral cerebellar ataxia
Leg wasting with absent reflexes and bilateral upgoing plantars
Posterior column signs (loss of vibration and propriocepiton)

Kyphosclolisos
Optic atrophy 
High arched palate
SN deafness
HOCM
DM
48
Q

Friedrich ataxia - genetics

A

AR
ONset teenage
Survival 20 years from diagnosis
Association with HOCM and DM

49
Q

Extensor plantars + absent knee jerks

A 
Friedrich ataxia
SCDC
MND
Taboparesis
Conus medullaris lesion 
Combined lower and upper pathology (e.g. cervical spondylosis with peripheral neuropahy
50
Q

Facial nerve palsy

A

U/L facial droop, involvement of forehead

VI+VII palsy - pons (MS/Stroke)
V+VI+VIII+cerebellar - cerebropontine lesion
VII + VIII - auditory/facial canal
Scars/parotic mass - tumour / trauma

51
Q

Commonest VII palsy

A

Bells - LMN
Rapid onset 1-2 days, HSV implicated
Swelling and compression within facial canal causes demyelination and temporary condution block
Prednisolone if started within 72h improves outcomes, acyclovir
EYE proteciton (tape, viscotears)
70-80% full recovery, remainder varying degrees of weakenss
More common in pregnancy

Other - VZV (ramsay hunt), mononeuropathy (DM, sarcoid, lyme), tumour/trauma, MS

52
Q

Bilateral facial palsy

A 
Guillain barre
Sarcoidosis 
Lyme disease
MG
B/L bells palsy
53
Q

Examining myaesthenia gravis

A

Bilateral ptosis worse on sustained upwards gaze
Complex bilateral extraocular palsies
Myaesthenic snarl
Bulbar - nasal speech, palatal weakness, poor swallow
Fatiguability
Sternotomy (thymectomy)
FVC

54
Q

Investigating myaesthenia gravis

A

Anti-AChR +ve in 90%
Anti-MuSK (muscle specific kinase) if Anti-AChr -ve
EMG - decremented response
Tensilon tests - an acetylcholine esterase inhibitor increases ACH at motor endplate to improve weakness (risks heart block or asystole)
CT - thymoma
TFTs (graves in 5%

55
Q

Treating myaesthenia gravis

A

Acute - IVIg or plasmapheresis is severe
Chronic - acetylcholine esterase inhibitors (pyridostigmine)
Immunusupression - steroids, azathiopine
Thymectomy - beneficial even if no thymoma

LEMS - diminished reflexes become brisker after exercise, lower limb girdle weakenss, SCLC association, Ab block voltage gated calcium channels, EMG

56
Q

Causes of bilateral extra-ocular palsies

A 
MG
Graves disease
Mitochondrial disease (e.g. Kearns-Sayre)
Miller Fisher
Cavernous sinus pathology
57
Q

Cause of bilateral ptosis

A 
Congenital 
Senile
MG
Myotonic Dystrophy 
Bilateral Horners
58
Q

Horners syndrome

A

Ptosis, miosis, anhydrosis, enothalmos
Look ipsilateral side of neck for scars - trauma, central lines, carotid endarterectomy, aneurysms, pancoast tumour

Brainstem - MS, stroke
Spinal cord - syrinx
Neck - aneurysm, Pancoast tumour

59
Q

Holmes Adie pupil

A

Myotonic pupil
Moderately dilated pupil with poor light response and a sluggish reaction to accomodation
Absent or diminished ankle and knee jerks
Benign condition

60
Q

III palsy

A

Down and out
Ptosis (usually complete)
Pilated pupil

Medical - pupil normal
- Mononeutritis multiplex (DM), midbrain infarct (webers) or demyelination, migraine)
Surgical - pupil blown
- posterior communicating artery aneurysm, cavernous sinus thrombosis, tumour or fistula, cerebral uncal herniation

61
Q

Compression of the cord

A

Myelopathy

62
Q

Compression of the nerve roots

A

Radiculopathy

63
Q

Ddx myelopathy

A

Sudden - vascular (spinal infarcts), disc prolapse

Inflammatory - MS, transverse myelitis

64
Q

Transverse myelitis

A

Immune - MS, post infectious, paraneoplastic
Viral - VZV, EBV, CMV, HSV
Bacterial - TB

65
Q

Assessing double vision

A

Does the double vision disappear when covering either eye = biocular diplopia
Is the double vision horizontal or vertical? Horizontal diplopia: lateral / medial rectus (unilateral / bilateral VI or INO) Vertical diplopia: superior / inferior rectus, superior / inferior oblique (III or IV)
Is the double vision worse on looking in any particular direction?
Diplopia is maximal in the direction of action of the paretic muscle

66
Q

Surgical Sieve

A

INVITED MD

Infection
Neoplasia
Vascular Inflammatory/autoimmune
Trauma
Endocrine
Degenerative
Metabolic
Drugs
Congenital
67
Q

Sturge Weber Syndrome

A

Port wine stain - classically V1 and v2 facial distribution
Leptomeningioma
Seizures
Glaucoma

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