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DPD > More neurological conditions > Flashcards

More neurological conditions Flashcards

1
Q

what are the major categories of neurological disease and how can you differentiate them

A
  • infectious
  • traumatic
  • congenital/genetic
  • vascular
  • degenerative
  • toxic
  • metabolic (acquired/inherited)
  • neoplastic
  • inflammatory/immune

Degenerative disease – slow - yrs

Vascular and trauma are fast

Inflammatory/autoimmune/neoplastic – subacute – mo

demographic

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2
Q

where is the problem if you have UMN signs

A

From cortex to subcortex to pyramidal decussation to spinal cord

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3
Q

distinguishing factors for facial weakness

A

UMN = forehead sparing - bihemispheric innervation of both nuclei for the frontalis muscle

Bell’s - eye cant open properly, white of eye seen when try and open it

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4
Q

where does the facial nerve sit

A

in the pons

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5
Q

summarise the visual pathway

A

doesn’t go through the brainstem, it goes above it

optic nerve -> optic chiasm -> radiation -> occipital lobe

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6
Q
A

Area of hypodensity = infarct

Middle cerebral artery

L middle cerebral artery territory infarct.

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7
Q

aphasia

A

expressive - cant produce the word they want to produce.

Receptive – cant understand what other people are saying to them ie cant follow commands

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8
Q

dx

A

MND

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9
Q

what is MND

A

degenerative condition - anterior horn cells and upper motor neurons in spinal cord = mixed UMN and LMN signs

cause unknown

10% familial

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10
Q

epidemiology of MND

A

inciddence 2-4/100000

50-70yrs (can be any adult age)

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11
Q

presentation of MND

A

insidious onset (nearly always missed)

motor nerves only affected - UMN and LMN (can be just one initially, other features develop with time)

progressive

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12
Q

amyotrophic lateral sclerosis

A

typical presentation of MND (60%)

one limb initially - foot drop, clumsy weak hand

some wasting

fasiculations, brisk reflexes, extensor plantar responses

no sensory signs

progression over weeks/mo

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13
Q

bulbar MND

A

dysarthria and dysphagia - 30% of cases

bulbar and pseudobulbar sx

dysarthria -> tongue wasting

fasiculation

brisk jaw jerk

weakness of neck muscles

may be limb sx

progression more rapid than ALS

Px = 2yrs until death

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14
Q

where are the cranial nerves

A

At top of spinal cord have the medulla (bulbar) – in here have the CN 12 11 10 and 9

Pons – 5 7 6 8

Midbrain – 3 and 4

Above that – optic nerve and visual pathway and olfactory pathway.

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15
Q

difference between bulbar and pseudobulbar

A

bulbar - function in mouth and oropharynx eg dysarthria/dysphagia, absent gag reflex, tongue fasiculations, absence of jaw jerk

pseudobulbar - UMN bulber problem = dysarthria/dysphagia spastic tongue, exaggerated gag reflex

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16
Q

other MND presentations

A

primary lateral sclerosis - 5% - pure UMN onset

progressive muscular atrophy - 5% - pure LMN onset - flail limb appearance

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17
Q

Dx of MND

A

clinical - look for fasiculations

EMG/NCS - chronic nerve root denervation

imaging (MRI) - exlude other causes eg cervical/lumbar degenerative changes and myelopathy - cervical/thoracic/lumbar spine (brain sometimes)

exclude:

benign fasiculation syndrome

bulbar - cerebrovascular disease

multifocal motor neuropathy

hereditory spastic paraplegia

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18
Q

Mx of MND

A

no cure

riluzole - glutamate antagonist - extend LE (3-5mo)

palliative

nutrition

soft diet - excessive secretions/salvation

opiates/benzodiazepines

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19
Q

dx

A

MS

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20
Q

definition of MS

A

evidence of damage to the CNS that is disseminated in time and space

damage occurs at different dates and to different parts of the CNS

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21
Q

pathophysiology of MS

A

immune mediated

  • T cell trigger attacks on myelin in CNS (inc optic nerve)
  • scarring caused by inflammatory attacks at multiple sites in CNS
  • plaques visible on MRI and autopsy

genetic predisposition with environmental triggers

  • 20% MS sufferes have blood relative with MS
  • low vit D, ENBV, smoking, extremes of latitude, obesity in adolescence
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22
Q

MS sx and signs

A

vary between people

  • fatigue
  • visual problem
  • bladder and/or bowel dysfunction
  • sexual dysfunction
  • emotional disturbances - depression, mood swings
  • cognitive difficulties - memory, attention, processing
  • sensory changes - tingling, numbness
  • pain - neurological, musculoskeletal
  • spaticity
  • gait, balance, and coordination problems
  • speech/swallowing problems
  • tremor (if cerebellar effected)
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23
Q

presentation of MS

A

Some presentations short lived – weeks/mo – vision loss/numbness – patient doesn’t report, battle between immune response and recovery.

Some get single episode of inflammation and some more progressive

loss of vision in 1 eye, with painful eye movements (optic neuritis)

double vision - brainstem syndromes

sensory disturbance or weakness, spastic parapesis, weakness and gait, increased tone and clonus, hyperreflexia -spinal cord lesion, transverse myelitis

balance related problems or clumsiness - cerebellar

altered sensation travelling down back when bend neck forward - Lhermitte’s syndrome

24
Q

Dx of MS

A

clinical

PMHx and Ex

evidence of damage disseminated in time and space

McDonalds critera - more reliant on MRI appearances of plaques

  • MRI - hyperdense plaques - Pathognomonic in corpus collosum
  • LP - in CSF see abnormal Ig present, or immune response in the CSF
  • visual evoke potentials - optic nerve slowed down by loss of myelin
25
Q

clinical course of MS

A

in young adults <40yrs

4 patterns of disease:

  • relapsing remitting - most common, gets better but return to worse baseline
  • primary progressive - worse Px
  • secondary progresive
  • progressive-relapsing remitting MS
26
Q

Mx of MS

A

neurology annual review

MDT

look for incection in relapse - IV or PO steroids

disease modifying drugs eg B interferon when not in relapse as prophylaxis

27
Q

dx of parkinson’s

A

clinical

28
Q

summarise parkinson’s

A

idiopathic

substantia nigra degeneration -> dopamine deficiency in striatum/basal ganglia -> motor sx = abnormality of movement, not loss

basal ganglia fasicilitates movement normally - extrapyramidal tract

dopaminergic therapy relieves motor sx

29
Q

3 cardinal sx of parkinson’s

A

tremor - high frequency resting tremor (5movements/sec) - pinrolling (finger and thumb), or supination-pronation

rigidity - different from increase in tone/spasticity in UMN. In spasticity – tone more notable in particular dirn. Parkinsons – leadpipe rigidity – equal in both directions.

Cogwheel rigidity – tremor superimposed on the tone.

Bradykinesia – don’t blink very often, paucity of movement, gait. Get them to tap fingers and see if it is slow

30
Q

features of parkinsons

A

Freeze when mobilise

Shuffling hait

Poor arm swing on one side

Poor posture

Problem swallowing postural hypotension, bowel and urinary function

Hypophonia

Need 2/3 of bradykinesia, tremor, rigidity

31
Q

causes of parkinsonism

A

parkinson disease - idiopathic or genetic

parkinson-plus degenerations

drug induced parkinsonism

vascular parkinsonism

brain trauma

CNS infection

32
Q

parkinson-plus degenerations

A

progressive supranuclear palsy - impaired gaze (cant look down), balance and dysarthria

multiple system atrophy - autonomic issues, urinary problems and orthostatic hypotension

33
Q

drug induced parkinsonism

A

anti-dopaminergics

drugs that reduce dopamine transmission - antipsychotics/antiemetics:

  • resperidone
  • haloperiodol
  • metoclopramide
34
Q

ways to differentiate Parkinson’s disease from other causes of parkinsonism

A

asymmetrical findings

no atypical features - eye fine, automomic shlouldnt be the predominant sx

not on/had neuroleptics

responds to L Dopa

35
Q

Mx of Parkinson’s disease

A

L-dopa (with carbidopa) - most effective and best tolerated

dopamine agonists - ropinirole, pramiplexole

MAO-B inhibitors, anti-cholinergics, amantadine have modest benefits

drugs are for sx relief, not neuroprotective/neurotoxic

response to L dopa is best diagnostic test for PD

36
Q

L-Dopa SE

A

non-motor:

  • nausea
  • orthostasis
  • sleepiness
  • hallucinations

dyskinesias

37
Q

Mx of PD as disease progresses

A

more motor complications as disease progresses - including dyskinesias and on-off fluctuations

drug resistant motor sx - impaired balance with falls

non-motor sx - dementia and hallucinations

38
Q
A

hemiplegic

typical of pyramidal weakness from stroke or UMN problem

Corticospinal tract affected – reflex arc exaggerated and out of control – spasticity in pyramidal pattern

Everything flexed in upper limb and extend in lower limb

swing leg out to prevent the foot drop

Hemiplegic stroke – extended position and arcs outward

39
Q

highstepping gait

A

foot drop - lift foot high so dont rip

40
Q

stomping gait

A

sensory problem – have to stomp so you get vibration – peripheral neuropathy

41
Q
A

Hoffman’s sign

42
Q

antalagic gait

A

painful leg - compensate by lifting leg up a bit

43
Q
A

L occipital lobe = R sided homonymous hemianopia

44
Q

sx to check for with visual field defects

A

clarify field of vision loss in transient sx

any positove phenomona

any associated sx

45
Q

dx

A

MS – internuclear ophthalmoplegia (INO) – brainstem and medial longitudinal fasiculus – associated with MS.

R eye didn’t adduct, L eye looked like it had nystagmus. Relate to the midbrain and pons – plaque occur in MS

46
Q
A

BPPV

Very short lived period of vertigo, related with head movement.

Manouvre – Dix-Hallpike gold standard test

Epley manouvre to make them feel better

47
Q
A

fatiguability

Myasthenia gravis

Eye becomes misaligned with other eye = squint – fatiguability

Diplopia in evening

And speech in consultation

48
Q

summarise myasthenia gravis

A

autoimmune synapto-pathy affecting NMJ of skeletal muscle

affecys ocular, face and swallowing

sx and signs worse with use - fatiguability

NCS and Ab testing - AChR and MUSK Ab test

CXR - thyoma, ice test

49
Q

Mx for myasthenia gravis

A

ACh inhibitors

immunosuppresssion

plasmapharesis and IVIG

surgery? thymectomy

50
Q
A

R middle cerebral artery stroke

51
Q
A

Cerebral met

Think about the mode of onset

SAH – all or nothing event – thunderclap headache

TIA – resolves in <24hrs

Cerebral infarct – wouldn’t progress – over mo language would get better.

52
Q
A

R brainstem:

Not cervical spine because face problem – and tracks above this

Not occipital – because would be vision of R of both eyes

R motor cortex – L sided face weakness

Have crossed signs here – face not equating to the body

Very typical for brainstem - Nucleus on one side, then pyramidal decussation

53
Q
A

spinal cord

54
Q
A

T10

55
Q
A

GBS

Ascending motor radiculopathy

Peripheral = areflexia

56
Q
A

Contact the stroke team – do scan where pt get treatment

57
Q
A

L cerebellum – cerebellum is ipsilateral innervation – L sided coordination.

DPD (38 decks)

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