Neurology Flashcards
1
Q
BENZO S/e
A
sedation resp depression Agitation ataxia sudden w/d - seizure tolerance
2
Q
phenytoin s/e
A
HYPERPLASIA GIGIVAL Hirtuism decrease BMD decrease folic acid drownsiness rash nystagmus
3
Q
Primidone
A
biotransformation into metabolites phenobarbitone and phenylethylmalonamide → anticonvulsant activity
Use: GP FEM generalisedseizures, psychomotor (temporal lobe) epilepsy, focal seizures, myoclonic jerks
Adverse effects: Decreased bone mineral density, ataxia, drowsiness, fatigue, hyperirritability, suicidal ideation, vertigo, rash, GI upset, impotence, haematological, nystagmus, diplopia
Comments: May reduce effectiveness of hormonal contraception
4
Q
s/e CARBAMAZEPINE
A
hyponatraemia, rash, pruritus, fluid retention, aplastic anaemia, hepatotoxicity, GI effects, sedation, ataxia, nystagmus, depression, dizziness, diplopia, lethargy, headache, idiosyncratic
May make primary generalised epilepsy worse.
5
Q
Valproate moa and s/e
A
inhibits na channel S/e - NTD - PCOS = hypothyroidism = insulin resistent DM
6
Q
ETHOSUXAMIDE moa and s/e
A
nausea, vomiting, sleep disturbance, drowsiness, and hyperactivity
Comments: Rarely lupus-like reactions, SLE
MOA: iBlocks T-type calcium channels in thalamic neurons
7
Q
lamotrigine s/e moa
A
Rash (Stevens-Johnson), tremor, headache, GI, insomnia, somnolence
moa blocks Na and decrease electrical emission
8
Q
how is VIGABATRIN secreted
A
really
9
Q
VIGABATRIN s/e
A
Sedation, fatigue, depression, psychosis,, headache, dizziness, weight gain
10
Q
TOPIRAMATE s/e
A
Sedation, cognitive slowing, renal stones, weight loss, glaucoma, paresthesias, headache, fatigue, dizziness, depression, mood problems, metabolic acidosis
11
Q
gabapentine moa and s/e
A
increase GABA in the brain binds to voltage dependent calcium channel
edation, dizziness, ataxia, GI upset, weight gain.
12
Q
TIAGABINE moa and s/e
A
GABA uptake inhibitor
potential pro-convulsive effect
Dizziness, tiredness, mood changes, lack of energy, somnolence, nausea, nervousness, TREMOR , DIFFICULT CONCENTRATION , abdominal pain
13
Q
ZONISAMIDE moa and s/e
A
blocks voltage-dependent sodium and T-type calcium channels
Somnolence, ataxia, cognitive slowing, weight loss, rash, ataxia, anorexia, confusion, abnormal thinking, nervousness, fatigue, and dizziness, nephrolithiasis (low risk)
14
Q
what two anticonvulsants cause nephrolithiasis
A
ZONISAMIDE
TOPIRAMATE
15
Q
LEVETIRACETAM moa s/e
A
Unclear, binds to a synaptic vesicle protein, may modulate synaptic transmission through alteration of vesicle fusion, may indirectly modulate GABA
Usually well tolerated
Sedation, mood disturbance, behavioural disturbance, fatigue, somnolence, dizziness, and infection (upper respiratory
16
Q
what anticonvulsants mess the OCP effectiveness up
A
phenytoin
Primidone
Carbamazepine
lamotrigine
17
Q
what three anticonvulsants are excreted renally vs. hepatic
A
- VIBigatrin
- Zonisamine
- Gabapentine
4/ levetiracetam
18
Q
Ulnar nerve Supplies and defect if damage
A
C8 , T1 supplies All small muscles of hands except LOAF Wasting of small muscles of hand Claw hand Sensory loss over medial one and half fingers Froment’s sign
19
Q
Radial nerve Supplies and defect if damage
A
C5-C8 Supplies Triceps Brachioradialis Extensors of hand Wrist drop Sensory loss over anatomical snuffbox
20
Q
Median nerve
A
C6-T1 Supplies Muscles of forearm (except FCU, FDP) LOAF Sensory loss over palmar aspect of thumb and lateral two fingers Ochsner’s clasping test Tinel’s test Phalen’s test
21
Q
Sciatic nerve
A
Supplies Hamstrings All muscles below knee Footdrop Weak knee flexion Normal knee jerk, absent/weak ankle jerk Sensory loss posterior thigh, lateral and posterior calf and foot
22
Q
Common peritoneal nerve
A
L4-S1 Terminal branch of sciatic nerbe Supplies Anterior and lateral leg compartments Weak dorsiflexion/eversion Normal reflexes Sensory loss lateral dorsum of foot
23
Q
Brown Squard Syndrome
A
IPSILATERAL - UMN sign below lesion, LMN at level of lesion and VIBRATION AND propioperception
CONTROLATERAL temp and pain
24
Q
SACD spinal cord
A
Symmetrical UMN signs in lower limbs Exaggerated knee jerks Absent ankle jerks Symmetrical proprioception/vibration loss Peripheral neuropathy Optic atrophy
25
CAUSE OF SACD SPINAL CORD
B 12
26
SYRINGOMYELIA
A fluid-filled, gliosis-lined cavity within the spinal cord
Pain/temperature loss over neck/shoulders/arm (cape)
Arm atrophy
UMN lesions in LL
Causes
Congenital malformations (e.g. Chiari malformation Type 1)
Postinfectious
Postinflammatory (e.g. transverse myelitis, MS)
Posttraumatic
27
CONUS MEDULARIS
Lesions at vertebral level L2
flaccid paralysis of the bladder and rectum
impotence
saddle (S3-S5) anaesthesia, usually more localised to perianal area.
Causes
disc herniation
spinal fracture
Space occupying lesion
28
seizure
sudden change in behaviour or function due to neurological dysfunction
epilepsy - recurrent seizures (at least 2) due to excessive electrical activity in the brain
29
Complication of epilepsy
```
AAA CDD T
AED S/e
anorexia
Acidosis
Cognitive impairment
Depression
death
Trauma / personal injury
```
30
Risk of epilepsy recurrence
- structural brain disease
- cognitive impairment
- multiple seizure type
- age onset in 1st decade ( 10 years)
- family history
- not responding to treatment
- combo treatment needed
- abnormal neuro exam
- epileptiform foci on EEG
- Abnormal MRI
31
Seizure biomarkers
```
CLP
cortisol
creatinine kinase
LDL
Prolactin
Ph
```
32
provocation testing for seizures on EEG
- sleep deprivation
| - hyperventilation
33
what classification is used for seizure
ILAE 2010
34
definition of MND
Progressive group of neurological conditions which affects motor neurons at the anterior horn cell. characterized by both UMN and LMN lesions and sensory invovlemt is unlikely
35
what does bulbar involvement mean
Means the medulla is affected and it involves CN 9-12
| RESULTS IN : dysarthria, dysphasia and laryngospasm
36
pathogenesis of MND
```
Nerve damage and loss
Both axonal and myelin damage
Subsequent gliosis occurs
Spinal cord atrophy
Muscle atrophy
Intracellular inclusions
```
37
Epidemiology of MND
2 types
- sporadic
- Familial - SOD1, TARDBP , CaORFT2
OLDER AGE
38
what are the additional symptoms you can get in MND
1. Cognitive impairment - 3 types: 1. Pseudobulbar palsy
dementia and
frontal Temporal lob (executive function and memory
2. Autonomic dysfunction
- falls
- urinary retention - catheter - recurrent UTI
- constipation - bowl obstruction
3. Parkinsonian features
4. Sensory - complain 20%, but no exam finding
39
UMN and LMN symp in MND
UMNL
- stiffness (HEAVY , Dragging)
- clonus
- spasm
LMNL
- weakness and atropin
fasciculation
cramps
40
UMN and LMN signs in MND
```
UMN
Spasticity
Slowed rapid alternating movements
Increased reflexes
Gait disorder
Spastic
```
```
LMN
Weakness
Gait disorder
Reduced reflexes
Muscle atrophy and fasciculations
```
41
Distal spread UMNL
contraction of muscles that produce motions other than the one associated with the test muscle
42
Hoffman’s sign
tapping the nail or flicking the terminal phalanx of the middle or ring finger. A positive response is seen with flexion of the terminal phalanx of the thumb.
43
Crossed adduction
contraction of the adductors of the thigh and inward rotation of the limb elicited by tapping the sole.
44
Triple flexion
Flexion at the hip, knee, and ankle, in response to stimulation of the sole of the foot.
45
palmomental sign
stroke palm see twitching - bulbar uMN L
46
ALS pulse syndrome
```
Frontotemporal dementia,
Autonomic dysfunction
Parkinsonism
Supranuclear gaze paresis
Sensory loss
```
47
Ddx MND
1. multifocal motor neuropathies
2. multifocal myopathies (dermatomyositis, polymyositis)
3. Hereditary neuropathies (hereditary spastic paralysis, spinobulbar muscular dystrophy)
4. inflammatory neuropathies (incision body myositis)
Others:
post polio syndrome
paraneoplastic (ovaries, lung, renal)
48
Exclusion Criteria
Clinical or electrophysiological - suggest other condition (e.g.hx of poliomyelitis)
Neuroradiological evidence of a condition that could otherwise account for the clinical syndrome (e.g. evidence of cervical myelopathy)
Failure of the condition to progress
49
El escorital criteria
LMN degeneration by clinical, electrophysiological, or neuropathological examination
UMN degeneration by clinical examination
Progressive spread
50
investigation of MND
```
Electrophysiology (EMG)
- fibrillation
- positive sharp waves
Nerve Conduction studies (do repetitive test to look for fatiguability)
potential
Imaging
Blood and CSF analysis - HIV, Septic screen, serum cA2+, TFT, SPEP and LP
MRI BRAIN
```
51
investigation for complication of MND
1. RESPIRATORY FUNCTION
2. MSU - infection
renal US - stone
3. full swallow assessment (video fluoroscopy)
4. Constipation - PFA
52
treatment
1. RILUZOLE
2. Symptoms:
Spasticity - Baclofen, Tizanidine
Cramping & fasciculation - Quinine sulphate
Salivation & drooling - Amitriptyline,Scopolamine, irradiation
Pseudo bulbar affect - Amitriptyline
3. Resp dysfunction - NIV
4. Swallow difficulty - thicken fluids, NPO, peg
53
long term survival in MND
Younger
male
limb symptoms (better than bulbar)
54
resp symp in MND that may be missed
```
Breathnessness
Early morning headaches
Daytime sleepiness, nocturnal agitation
Nightmares
Confusion
```
Hypoxic signs
55
Chorhea 2 types
Athetosis - slower, writhing movements
| Ballism - proximal and large amplitude
56
Dystonia
Involuntary, sustained muscle contractions that result in twisting and repetitive movements or abnormal posture. [2]
57
tic
Brief, repeated, stereotyped movements which patients can suppress for a period of tim
58
Myoclonus
Brief, shock-like, involuntary movements caused by muscular contractions or inhibitions
59
Tardive Dyskinesia
Orobuccolingual, truncal or choreiform movements (grimacing/chewing)
Chronic exposure to antipsychotics/antiemetics (dopamine receptor blockers)
60
4 hypokinesia disorders
Parkinsons
Progressive nuclear palsy
Portico-Basal degneration
Multiple system atrophy
61
wha trinucelar repeat in fridrich's ataxia
GAA
62
hereditary spinocerbral ataxia
progressive cerebellar syndrome
| oculomotor retinal and pyramidal EP sensory cognitive and behavioural sam
63
what trinucelar repeat for huntigton
CAG
64
multiple sclerosis
immune-mediated inflammatory disease of the central nervous system, characterised by demyelination
65
proven risk factors
```
Female gender
age 25-35
other A.I disease
MHC 1 and 2 alleles
HLA DRB1
MZT concordance: 20-40%
```
66
what is a relapse in MS called
Episode of neurological dysfunction lasting >24 hours in the absence of fever
Often lasts weeks to months
May gradually improve (remission)
May have residual disability following relapse
67
disseminated in space
```
Dissemination in space requires
≥1 T2 bright lesions in 2 or more locations:
- Periventricular
- infratentorial
- juxtacortical
- spinal cord
```
68
Dissemination in time
Dissemination in time can be established in one of two ways:
1. a new T2 bright lesion and/or gadolinium-enhancing lesion when compared to a previous scan (irrespective of timing)
2. presence of asymptomatic enhancing lesion and a non-enhancing T2 bright lesion on any one scan
69
B-interferon S/e
site necrosis, flu-like symptoms, abnormal LFTs (ALT), leukopaenia, anaemia
70
Gatiramer-acetate
injection site-reaction, post-injection chest pain, flushing, dyspnoea, palpitations, and/or anxiety
71
Natalizumab moa s/e
evelopment of progressive multifocal leukoencephalopathy
T cell lymphocyte inhibitor
72
Alemtuzumab S/e and moa
depletion of CD52
-expressing T cells, B cells, natural killer cells, and monocytes
S/e autoimmune disorders, including immune thrombocytopenia
73
Mitoxantrone s/e and use
Side-effects: cardiotoxicity, immunosuppression, possible link with colorectal Ca
USE Reserved for patients with rapidly advancing disease who have failed other therapies
74
Dimethyl Fumarate (oral)
neuroprotective and immunomodulatory properties
flushing and gastrointestinal symptoms, lymphopaenia, PML
75
Teriflunomide (oral)
disrupts the interaction of T cells with antigen presenting cells
diarrhoea, nausea, hair thinning, hepatotoxicity, teratogenicity
76
Fingolimod (oral)
alters lymphocyte migration, sequestration of lymphocytes in lymph nodes
small increased risk of infection, atrioventricular block, and possibly basal cell carcinoma.
77
spasticity in MS treatment
Baclofen (may also be given via intra-thecal pump)
Tizanidine :
Gabapentin
Clonazepam/diazepam: For cerebral-mediated spasticity
Botulinum toxin
Surgery: chronic epidural stimulation
78
Fatigue in MS
Amantidine
4 Aminopyridine
Antidepressnants
Modafinil
79
Bladder sphincter dysfunction
Anticholinergics/antimuscarinics
Botulinum toxin
Self intermittent catherisation
Suprapubic catheterisation
80
Bowel sphincter dysfunction
```
Laxatives
Pro-kinetics
Bowel stimulants
Bulking agents
Manual evacuation
```
81
Poor prognosis of MS
```
Early onset
High lesion load
Short interval between relapse
Primary progressive MS
Bowel/bladder symptoms at onset
```
82
Muscular disease definition
Neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber
People with muscular disorders describe weakness doing specific movements (distinct from patients who complain of generalised weakness)
83
Ddx muscle weakness
```
CNS damage- Stroke, SOL
Spinal cord injury or disease
Anterior horn cell disease- MND, polio
Peripheral nerve disease
Neuromuscular junction disease- myasthenia gravis, Eaton Lambert syndrome
```
84
Myotonic dystrophy definition
Inherited (autosomal dominant) disease characterized by adult onset muscular dystrophy.
DM1: Trinucleotide repeat on chrom 19
DM2: tetranucleotide repeat - chromosome 3
85
Definition of myotonia
Slow relaxation of muscle following contraction (myotonia diminishes as disease progresses)
86
how to make diagnosis of muscle dystrophy
Genetic testing
CTG repeat in DM1
CCTG repeat in DM2
```
EMG
repetitive myotonia (sounds like “dive-bomber”)
Predominant in distal muscles
```
Muscle biopsy
Atrophy
Necrosis
Increased nuclei
87
signs of myotonic dystrophy
Finger grip myotonia- delay in letting go when shaking hand, or delay in loosening grip when asked to grips fingers
Percusssion myotonia- tapping over thenar eminence causes
Distal muscle weakness
Impaired extra-ocular muscle usage
Gynaecomastia
CF of cardiomyopathy- displaxed apex, murmurs, crepitations, etc.
Testicular atrophy
88
Ddx : TIA
```
Migraine
Partial Seizure
Syncope
Vestibular Disorders
Neuropathy and Radiculopathy
Ocular Disorders
Hypoglycaemia
CNS Tumours
```
89
ABCD2 score
Age > 60
Blood Pressure > 140/80
Clinical (2 points for hemiparesis , 1 point for speech problem w/o weakness)
Duration 2 points > 60 minutes, 1 point 10-60 minutes
Diabetes
90
Interpretation of ABCD2 score
Score 6 to 7: High two-day stroke risk (8 percent)
Score 4 to 5: Moderate two-day stroke risk (4 percent)
Score 0 to 3: Low two-day stroke risk (1 percent)
91
Agnosia
inability to interpret sensation
92
MCA stroke presentation
```
Contralateral paralysis (Face and limbs)
Contralateral sensory loss (Face and limbs)
Aphasia/Dysphasia
Homonymous hemianopia
Agnosia
Sensory neglect
Apraxia (dressing/constructional)
```
93
Apraxia
Apraxia (dressing/constructional
94
Agnosia
inability to interpret sensation
95
Abulia
inability to act decisively
96
Posterior cerebral artery stroke
```
CENTRAL
Mild hemiparesis
Choreathetosis
Intention tremor
Thalamic syndrome- simultaneous sensory loss and anaesthesiae/parasthesiae
```
```
PHERIPHERAL
Homonymous hemianopia/quadrantanopia
Visual neglect
Visual apraxia
Prosopagnosia
Visual hallucinations
Memory abnormalities
```
97
BP should only be treated acutely in stroke if:
```
BP should only be treated acutely if:
Patient is candidate for thrombolysis
Severe HTN (SBP>220mmHg, DBP > 120mmHg)
Co-existing ACS, AKI, acute CCF, acute aortic dissection
Haemorrhagic stroke
```
Otherwise a higher BP - tolerated in ischemic stroke its permissive HTN
98
Lateral Medullary Syndrome
```
Ipsilateral
Facial pain
Impaired facial/limb sensation
Nystagmus
Ataxia
Vertigo
Diplopia
Oscillopsia
Impaired gag reflex
Dysphagia
Horner’s syndrome
```
Contralateral -Impaired pain and temperature sensation
99
Posterior cerebral artery stroke
```
CENTRAL
Mild hemiparesis
Choreathetosis
Intention tremor
Thalamic syndrome- simultaneous sensory loss and anaesthesiae/parasthesiae
```
```
PHERIPHERAL
Homonymous hemianopia/quadrantanopia
Visual neglect
Visual apraxia
Prosopagnosia
Visual hallucinations
Memory abnormalities
```
100
BP should only be treated acutely in stroke if:
```
BP should only be treated acutely if:
Patient is candidate for thrombolysis
Severe HTN (SBP>220mmHg, DBP > 120mmHg)
Co-existing ACS, AKI, acute CCF, acute aortic dissection
Haemorrhagic stroke
```
Otherwise a higher BP - tolerated in ischemic stroke its permissive HTN
101
blood pressure is >185/110 mmHg, treat with:
Labetalol IV, up to twice OR
| Nicardipine drip
102
Malignant MCA syndrome
```
2-5 days post stroke
Mortality 50-80%
Clinical Predictors:
Young age
History of hypertension, heart failure,
Raised WCC,
Coma on admission
Nausea, vomiting
SBP> 180mmHg within first 24hrs
```
103
criteria for hemicrainectomy
- Age< 60
- NIHSS>15
- Decrease LOC >/=1 on item 1a of the NIHSS
< 45 hrs from onset(surgery should be undertaken < 48hrs from onset)
- space occupying cerebellar infarcts
- At least 50% MCA territory involved on CT, with / without additional infarction in the territory of the anterior or posterior cerebral artery on the same side, or 145cm3 on DWI MRI
104
what location of stroke is worse
ACA and PCA
| Best = lacunar
105
prognosis post stroke
Severity of stroke (NIHSS scale)
Site of stroke
co-morbidities,
Baseline function
Presence of continued risk factors (smoking, poor DM control, AF, etc.)
BMI - low or normal BMI confer poor prognosis
106
treatment of heamorragic stroke
Reversal of anticoagulant
- ABC, Tx infection, Early SALT review, BP monitor, seizure prophylactic,
Possible craniotomy
107
what is better for stroke CT OR MRI
```
Non-contrast CT brain ±CT angiogram (intracranial ± carotids/vertebrals)
MRI brain (more sensitive for early infarct with FLAIR, less widely available)
```
