neurology Flashcards
define epilepsy
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.
What are the types of generalized seizures you can get?
tonic clonic absence atonic tonic clonic myoclonic
tonic clonic seizure
tonic ( rigid as muscles contract) and then convulse making rhythmical muscular contractions (clonic).
absence
petit mal normally occurs in children
patient loses consciousness and appears vacant and unresponsive to observers forup to 30 sec
atonic
brief loss of muscle tone patient falls to the ground
tonic
sustained muscle contraction
clonic
rhythmic muscular contractions
myoclonic
an extremely brief muscular contraction less than .1 of a second seen as a jerky movement.
what is a partial seizure?
divided into simple (conscious) or complex ( impaired consciousness) . It can be then subdivided based upon the brain area affected temporal frontal parietal or occipital
partial seizure temporal lobe
deja vu, jamais vu, olfactory/ auditory aura, epigastic discomfort.
partial seizure- frontal lobe
motor
partial seizure - parietal
sensory (crawling up arm)
occipital partial seizure
visual
SE of anticonvulsants common to all
(Na valproate, phenytoin, carbamazepine, lamotrigine) ALL are teratogenic
Na valproate SE (repro)
associated with neural tube defects
pheytoin SE (repro)
cleft palate and congential heart disease, interfere with the OCP so should double dose or use barrier methods.
Na valproate
weight gain hair loss and curling, nausea, vomiting, drug induced hepatitis, rash, drowsiness, tremor
lamotrigine
rash (steven johnson syndrome, headaches, dizziness, insomnia, vivid dreams.
carbamazepine SE
rash, nausea, atazia, diplopia, agranilocytosis, hyponatremia
phenytoin SE
acne, rash, atazia, ophalmoparesis, sedation, gingival hyperplasia
what is the law concerning driving with an episode of loss of conciousness
- simple faint with prodromal syndromes and a proking factor no restrictions
- due to transient loss of blood supply to the brain with a low risk of reoccurrence than can return in 4 weeks time.
- 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.
- if unexplained loss of conciouness than cannot drive for 6 months
- If seizure activity than cannot drive for one year.
limb weakness seconds to minutes
trauma (displaced vertebral fractures) or vascular insult (tia, stroke)
hours to days limb weakness ddx
progressive demyelination (guillian barre and MS) or slowly expanding subdural heamatoma
chronic weeks to months limb weakness
slow growing tumour or a motor neuron disease
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.
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
Why should you ask about seizures with the limb weakness?
seizures are associated with hypoglycaemia and also epilepsy (TODD’s paresis)
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
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.
where is the lesion in receptive dysphasia
wernicke area in the temporal lobe of the dominant hemisphere
where int he lesion in expressive dysphasia
broca’s area in the the frontal lobe of the dominant hemisphere
When the patient is not responding to stimuli on side of his body where is the lesion?
parietal cortex
complete blindness in one eye suggests
lesion is in the optic nerve
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)
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.
spinothalamic tract
pain and temp
dorsal column
light touch, proproception, vibration
In a LMN when the sensory sign present indicate
peripheral nerve lesion
in a LMN lesion with the sensory signs absent
nerve root lesion
What supplies the medial part of the cerebral cortex.
The motor cortex for the lower limbs is by the anterior cerebral artery
What supplies the lateral portion of the motor cortex
hands, upper limb and face this is supplied by the middle cerebral artery.
Why can a infarct by the MCA cause contralateral hemineglect?
it supplies the posterior parietal cortex.
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
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.
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
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
What is a disability screen for a stroke patient?
GCS swallow speech and lang visual fields gait
What is risk factor reduction in a patient with hx of stroke and also a carotid bruit?
carotid endarterectomy
also quite smoking
drug prophylaxis in stroke patients?
- antiplatelet: clopidogrel daily
- daily statin: even if the cholesterol levels are normal
- 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
What is the stroke framework?
Time course deficit location disease aetiology
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
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
In the TIA clinic what investigations are they going to do?
- history looking for any modifiable risk factors: smoking hypertension, hyperlipidemia, D.M
- examination: carotid, pulse
- bedside ECG AF
- bloods: glucose, FBC, clotting profile
- imaging: MRI brain
When to use antiplatelets?
useful in clots that form due to endothelial activation of platelets (atheroscerotic plaques) prevent MI and primary ischeamic stroke
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.
What two scoring systems can you use to determine the benefit of coagulation therapies or antiplatelet therapies?
CHA2DS2 VASC score and the HASBLED score
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.
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
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
Brown sequard syndrome explain anatomically
each half the spinal cord contains
- UMN innervating the ipsilateral side of the body
- dorsal column neurons (vibration, prop, and fine touch) innervating the ipslateral side of the body
- spinothalamic neurons (pain, temp, and light touch) innervating the contralateral side of the body.
