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neurology Flashcards

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1
Q

define epilepsy

A

Epilepsy is defined as a tendency to have recurrent unprovoked seizures. A single seizure is not enough to diagnose epilepsy. A seizure is defined as a transient excessive electricity in the brain that has motor, sensory, or cognitive manifestations discernible to the patient or observer.

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2
Q

What are the types of generalized seizures you can get?

A 
tonic clonic
absence
atonic 
tonic 
clonic
myoclonic
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3
Q

tonic clonic seizure

A

tonic ( rigid as muscles contract) and then convulse making rhythmical muscular contractions (clonic).

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4
Q

absence

A

petit mal normally occurs in children

patient loses consciousness and appears vacant and unresponsive to observers forup to 30 sec

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5
Q

atonic

A

brief loss of muscle tone patient falls to the ground

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6
Q

tonic

A

sustained muscle contraction

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7
Q

clonic

A

rhythmic muscular contractions

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8
Q

myoclonic

A

an extremely brief muscular contraction less than .1 of a second seen as a jerky movement.

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9
Q

what is a partial seizure?

A

divided into simple (conscious) or complex ( impaired consciousness) . It can be then subdivided based upon the brain area affected temporal frontal parietal or occipital

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10
Q

partial seizure temporal lobe

A

deja vu, jamais vu, olfactory/ auditory aura, epigastic discomfort.

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11
Q

partial seizure- frontal lobe

A

motor

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12
Q

partial seizure - parietal

A

sensory (crawling up arm)

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13
Q

occipital partial seizure

A

visual

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14
Q

SE of anticonvulsants common to all

A

(Na valproate, phenytoin, carbamazepine, lamotrigine) ALL are teratogenic

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15
Q

Na valproate SE (repro)

A

associated with neural tube defects

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16
Q

pheytoin SE (repro)

A

cleft palate and congential heart disease, interfere with the OCP so should double dose or use barrier methods.

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17
Q

Na valproate

A

weight gain hair loss and curling, nausea, vomiting, drug induced hepatitis, rash, drowsiness, tremor

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18
Q

lamotrigine

A

rash (steven johnson syndrome, headaches, dizziness, insomnia, vivid dreams.

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19
Q

carbamazepine SE

A

rash, nausea, atazia, diplopia, agranilocytosis, hyponatremia

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20
Q

phenytoin SE

A

acne, rash, atazia, ophalmoparesis, sedation, gingival hyperplasia

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21
Q

what is the law concerning driving with an episode of loss of conciousness

A
  1. simple faint with prodromal syndromes and a proking factor no restrictions
  2. due to transient loss of blood supply to the brain with a low risk of reoccurrence than can return in 4 weeks time.
  3. if syncope with high risk of reoccurrance can drive four weeks after event if cause ID and treated. If not identified than cannot drive for 6 months.
  4. if unexplained loss of conciouness than cannot drive for 6 months
  5. If seizure activity than cannot drive for one year.
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22
Q

limb weakness seconds to minutes

A

trauma (displaced vertebral fractures) or vascular insult (tia, stroke)

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23
Q

hours to days limb weakness ddx

A 
progressive demyelination (guillian barre and MS)
or slowly expanding subdural heamatoma
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24
Q

chronic weeks to months limb weakness

A

slow growing tumour or a motor neuron disease

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25
Why is time of onset of stroke SO important in the history taking?
because the window of time in which to confirm the dx and administer thrombolysis is only 4.5 hours from onset.
26
If there is a headache with the onset of limb weakness what would you be thinking of?
subarachnoid haemorrhage. unilateral headache may be hemiplegic migraine. gradual onset headache- slow growing tumour
27
Why should you ask about seizures with the limb weakness?
seizures are associated with hypoglycaemia and also epilepsy (TODD’s paresis)
28
What are the risk factors fro stroke that you should illicit in the history?
TIA, or past stroke, AF, atherosclerotic disease or RF | migraine with aura, and systemic lupus erythmatosus
29
How do you differentiate between an upper and lower motor neuron lesion?
``` upper motor neuron increased tone increased reflexes up going planters with babinski reflex and splaying of the toes clonus LMN decreased tone decreased reflexes fasiculations wasting. ```
30
where is the lesion in receptive dysphasia
wernicke area in the temporal lobe of the dominant hemisphere
31
where int he lesion in expressive dysphasia
broca’s area in the the frontal lobe of the dominant hemisphere
32
When the patient is not responding to stimuli on side of his body where is the lesion?
parietal cortex
33
complete blindness in one eye suggests
lesion is in the optic nerve
34
homonymous hemianopia
loss of the same half of the vision field in both eyes suggests a lesion between the optic chiasm and visual cortex (beware visual neglect can mimic this)
35
eye deviation
If the eye deviates away from the weak side this suggests a cortical lesion if the eyes deviate towards the weak side it suggests a brain stem lesion.
36
spinothalamic tract
pain and temp
37
dorsal column
light touch, proproception, vibration
38
In a LMN when the sensory sign present indicate
peripheral nerve lesion
39
in a LMN lesion with the sensory signs absent
nerve root lesion
40
What supplies the medial part of the cerebral cortex.
The motor cortex for the lower limbs is by the anterior cerebral artery
41
What supplies the lateral portion of the motor cortex
hands, upper limb and face this is supplied by the middle cerebral artery.
42
Why can a infarct by the MCA cause contralateral hemineglect?
it supplies the posterior parietal cortex.
43
What are the first line investigations in a stroke?
bedside: blood glucose to rule out hypoglycaemia ECG looking for AF bloods: FBC polycythemia, thrombocytosis, or thrombocytopenia clotting screen: if patient is on warfarin and to exclude a coagulopathy imaging: CT brain non contrast to rule out haemorrhage
44
If the patient has a confirmed ischeamic stroke but presents out side the thrombolysis window what can you do?
Anti platelet drug: aspirin stroke unit: MDT and speech therapy OT, physiotherapist VTE prophylaxis increased risk of thrombotic events PE or DVT low molecular weight heparin if haemorrhaging stroke has been excluded.
45
What are the second line investigations that are done on the stroke unit?
carotid doppler US: carotid artery atheromas that could be the source of emboli causing the stroke. ECHO: cardiac source of emboli or a patent foramen ovale
46
What are stroke patient in the ward more at risk of?
since they are immobile they need to be checked for pressure sores which can quickly become sources of infection. Regular moving of the patient is important. aspiration pneumonia stroke patients have difficulty swallowing- speech and lang carry out a swallow assessment and they may need NG tube VTE prophylaxis and recurrent ischeamic stroke
47
What is a disability screen for a stroke patient?
``` GCS swallow speech and lang visual fields gait ```
48
What is risk factor reduction in a patient with hx of stroke and also a carotid bruit?
carotid endarterectomy also quite smoking
49
drug prophylaxis in stroke patients?
1. antiplatelet: clopidogrel daily 2. daily statin: even if the cholesterol levels are normal 3. daily angiotensin converting enzyme *ACE inh* and or thiazide diuretic aiming for a blood pressure less than 130/85 or less than 120/80 if diabetic
50
What is the stroke framework?
``` Time course deficit location disease aetiology ```
51
What is the score used to assess risk in a TIA
ABCD2 score Age: 1 pt for greater than 65 blood pressure: 1 pt for grater than 140/90 clinical features: 1 pt for speech disturbance without weakness 2 pt for unilateral weakness duration of symptoms: 1 pt for 10-59 min 2 pt for greater than 60 diabetes 1 pt points greater than 4 need to be seen in 24 hrs at clinic
52
what if you don’t find the cause of the TIA and discharge the patient?
Then the patient is 25% likely to develop a TIA, stroke or fatal CVA. within 90 days
53
In the TIA clinic what investigations are they going to do?
1. history looking for any modifiable risk factors: smoking hypertension, hyperlipidemia, D.M 2. examination: carotid, pulse 3. bedside ECG AF 4. bloods: glucose, FBC, clotting profile 5. imaging: MRI brain
54
When to use antiplatelets?
useful in clots that form due to endothelial activation of platelets (atheroscerotic plaques) prevent MI and primary ischeamic stroke
55
When to use anticoagulants?
clots that form during blood stasis (deep vein thrombosis or AF) are rich in fibrin and erythrocytes. Need to be used by drugs that inhibit fibrin mesh formation.
56
What two scoring systems can you use to determine the benefit of coagulation therapies or antiplatelet therapies?
CHA2DS2 VASC score and the HASBLED score
57
What are the eye signs noted in patients with MS
*this can be on the other side but we will stick with one example for simplicity get the patient to go from extreme right graze to extreme left gaze the right eye is slow to adduct relative to the left and there is abnormal nystagmus of the left eye.
58
What are the imaging and investigations you can do in a patient with MS
Lumbar puncture for oligoclonal bands, it is characteristic to find elevated levels of multiple IgG antbodies IgG antibiotics are derived from B cell clones dark bands on clonal gel MRI brain and spinal cord looking for plaques (sclerotic- demyelonated) delayed response to visually provoked potentials
59
What are the contraindications for thrombolysis
``` onset not confirmed with 4.5 hours acute heamorrhage on CT scan seizure at the onset of stroke subarachnoid heamorrhage stoke/ head injury in the past 3 months major surgery/ trauma within 2 weeks previous ICH intracranial neoplasm arteriovenous malformation or aneurysm GI heamorhage LP in the past week platelets less than 100 INR less than 1.7 glucose less than 2.7 or greater than 22 pos. preg TIA systolic BP greater than 185 or diastolic greater than 110 suspected pericarditis ```
60
Brown sequard syndrome explain anatomically
each half the spinal cord contains 1. UMN innervating the ipsilateral side of the body 2. dorsal column neurons (vibration, prop, and fine touch) innervating the ipslateral side of the body 3. spinothalamic neurons (pain, temp, and light touch) innervating the contralateral side of the body.

Final Med (35 decks)

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