Flashcards in Neurology Deck (64)
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31
How are seizures classified?
PARTIAL - focal onset with features referable to one part of a hemisphere
Simple partial: awareness is unimpaired, focal symptoms with no post ictal phase
Complex partial: awareness is impaired. May have simple partial (aura) onset, or impaired awareness from the onset. Usually from the temporal lobe.
Partial seizure with secondary generalisation: after the initial partial seizure the electrical activity spreads more widely
PRIMARY GENERALISED - simultaneous onset of electrical discharge throughout the cortex. No localising features.
Absence: brief <10s, presents in childhood
Tonic -Clonic: loss of consciousness, limbs stiffen (tonic) and then jerk (clonic), post ictal phase and drowsiness common.
Myoclonic: sudden jerk of a limb face or trunk
Atonic: sudden loss of muscle tone causing to fall, no LOC
32
Multiple Sclerosis:
What is is?
How does it present?
How is it diagnosed?
Relapsing and remitted demyelinating disease of the CNS.
The plaques of demyelination occur at different sites, due to a T cell mediated response, unclear why. They heal incompletely causing the relapsing and remitting nature, with progressive neuronal loss.
The most common sites for plaques are:
optic nerves
periventricular region
corpus callosum
brainstem
cerebellar connections
cervical cord
33
Multiple Sclerosis:
What is is?
How does it present?
How is it diagnosed?
Relapsing and remitted demyelinating disease of the CNS.
The plaques of demyelination occur at different sites, due to a T cell mediated response, unclear why. They heal incompletely causing the relapsing and remitting nature, with progressive neuronal loss.
The most common sites for plaques are:
optic nerves
periventricular region
corpus callosum
brainstem
cerebellar connections
cervical cord
It is diagnosed clinically, and requires lesions to be disseminated in time and space, and unattributed to other causes. The McDonald Criteria is used.
MRI can show the lesions
CSF shows olioclonal bands of IgG that are not present in the serum.
Delayed Evoked potentials
34
What are the symptoms of MS as it progresses?
Cognition decline, including memory
Emotional liability
Decreased mobility and increased fatigue
Incontinence
Pain
Spasticity
Oscilliopsia
35
What is the definition of a TIA?
A sudden onset of focal CNS phenomena due to temporary occlusion of part of the cerebral circulation.
Symptoms last
36
What is amaurosis fugax?
Emboli in the retinal artery causing a curtain to descend over the vision in one eye.
37
What are the causes of TIAs
ATHEROTHROMBOEMBOLISM:
from carotids
suspect if many episodes on the same side
carotid bruit
May need carotid endarterecomy if stenosis >70%
CARDIOEMBOLISM:
Mural thrombus post MI or in AF
Need to anticoagulate
HYPERVISCOSITY
polycythaemia, sicklecell, high WCC, myeloma
VASCULITIS
cranial arteritis, PAN, SLE etc
very rare
?actually a TIA
38
What would lead you to an urgent referral to TIA clinic?
ABCD2 score
>6 indicates stroke in 2 days high risk
>2 need to be assessed within 24hrs
Everyone else needs to be assessed within 72hrs
Age >60 = 1 point
Blood pressure >140/90 = 1 point
Clinical features:
unilateral weakness = 2 points
speech disturbances but no weakness = 1 point
Duration :
>1hr = 2 points
10-59 mins = 1 point
Diabetes = 1 point
39
What is Guillian Barre Syndrome?
Acute autoimmune inflammatory demyelinating polyneuropathy.
40
What are the signs that would make you think a patient had Guillian Barre Syndrome?
Ascending weakness starting a few weeks after an infection, especially diarrhoea (campylobacter).
Loss of reflexes, mild sensory symptoms, cranial nerve involvement, autonomic dysfunction
Increased protein in CSF but not increased WCC.
Slow conduction on nerve studies
41
What test needs to be repeated regularly to monitor patients with Guillian Barre Syndrome?
FVC - needs to be checked every 4 hours to make sure that any respiratory muscle involvement is noted before it is difficult to intubate.
If FVC 6 consider ventilating.
42
Autonomic neuropathy:
Causes
Signs
Causes:
Diabetes, GBS, HIV, paraneoplastic syndrome, leprosy, SLE, toxic, genetic
Signs:
Postural hypotension, erectile dysfunction or ejaculatory failure (Point and Shoot), less sweating, constipation, nocturnal diarrhoea, urine retention, Horner's syndrome, Holmes-Adies pupil
43
What are the causes of polyneuropathy?
Mostly motor -
Guillian Barre syndrome
Lead poisioning
Charcot Marie Tooth syndrome
Mostly sensory -
Diabetes
renal failure
Leprosy
Others:
Hypothyroidism, hypoglycaemia, mitochondrial disorders
Vasculitides - polyarteritis nodosa, RA, wegeners
Malignancy
Infections - HIV, lymes
Nutritional - low B12 (EtOH), low folate, high vit B6.
Drugs - isoniazid, phenytoin, nitrofurantoin
Amyloidosis
44
What is the triad of parkinsonism?
Tremor - worse at rest
Rigidity - superimposed with tremor to cause cogwheel Bradykinesia - slowness of movement initiation with progression to reduction in speed and amplitude of repetitive movements
45
What are the causes of parkinsonism?
Idiopathic
Multiple cerebral infarcts
Parkinsons plus
Post encephalopathy
Drug induced - neuroleptics, prochlorperazine, metoclopramide
Toxin induced
Trauma
46
What are the non motor features of Parkinson's disease?
Anosmia
Depression
Dementia
Visual hallucinations
Dribbling
Postural instability
REM behaviour sleep disturbance
Mild urinary frequency and urgency
L dopa side effects
47
What medications can help in Parkinson's disease?
Levodopa (used with a dopa decarboxylase inhibitor)
Dopamine agonists - delays using LDopa
Anticholinergics - help tremor
MAO-B inhibitors - used in early PD
COMT inhibitors - may lessen OFF time
48
Huntingtons disease:
How is it inherited?
How does the disease progress?
What is the pathology?
It is autosomal dominant
Early symptoms are insidious: slightly twitching of muscles, clumsiness, lack of concentration, short term memory loss, depression, changes in mood.
It then progresses to chorea, dementia, fits and then death, within 15yrs of diagnosis.
Cerebral atrophy, with loss of corpus striatum GABA and cholinergic neurones.
49
What tracts do the different sensory modalities travel in the spinal cord?
Pain and temperature - spinothalamic
Joint position and vibration - dorsal columns
50
What are the differences between upper and lower motor neurone lesions?
UMN lesions:
Affects muscle groups
Pyramidal - extension of the upper limbs and flexion of the lower limb
Spasticity
Hyperreflexia
Up going plantars and clonus
LMN lesions:
Wasting and fasciculation
Hypotonia and reduced reflexes
51
How is muscle weakness graded?
0 - no muscle contraction
1 - flicker of contraction
2 - some active movement
3 - active movement against gravity
4 - active movement against resistance
5 - normal power
52
Which areas of the brain do the different cerebral arteries supply?
Anterior - frontal ad medial part of cerebrum.
Occlusion may cause weak, numb, contralateral leg and arm. Face is spared.
Middle - lateral part of each hemisphere.
Occlusion causes contralateral hemiparesis, hemisensory loss to face and arm. Contra lateral homonymous hemianopia
Posterior - supplies occipital lobe
Occlusion give contra lateral homonymous hemianopia with macula sparing.
53
What are the different types of tremor and what causes them?
Resting tremor - abolished on voluntary movement. Seen in Parkinson's
Intention tremor - irregular, large amplitude worse at the end of purposeful movement. Seen in cerebellar damage (MS, stroke)
Postural tremor - absent at rest, present on maintained posture, my persist but is not worse on movement. Seen as benign essential tremor.
Re - emergent tremor - postural tremor developing after a delay of ~10secs.
54
What conditions cause chorea?
Huntingtons and syndenhams chorea (post strep infection)
55
What are Hemiballismus?
Large amplitude, flinging hemi chorea contralateral to a lesion in the subthalamic nucleus
56
What is a dystonia?
A prolonged muscle contraction causing abnormal posture.
57
What are lacunar infarcts?
Small infarcts around the basal ganglia, internal capsule, thalamus and pons
58
What are the causes of TIAs
ATHEROTHROMBOEMBOLISM:
from carotids
suspect if many episodes on the same side
carotid bruit
May need carotid endarterecomy if stenosis >70%
CARDIOEMBOLISM:
Mural thrombus post MI or in AF
Need to anticoagulate
HYPERVISCOSITY
polycythaemia, sicklecell, high WCC, myeloma
VASCULITIS
cranial arteritis, PAN, SLE etc
very rare
?actually a TIA
59
What test needs to be repeated regularly to monitor patients with Guillian Barre Syndrome?
FVC - needs to be checked every 4 hours to make sure that any respiratory muscle involvement is noted before it is difficult to intubate.
If FVC 6 consider ventilating.
60
