Neurology Flashcards
(64 cards)
What domains make up the Glasgow coma score?
Eye Opening:
- none
- to pain
- to speech
- spontaneous
Best motor response:
- None
- extension to pain
- flexion to pain
- withdraws from pain
- obeys commands
Best verbal response:
- none
- incomprehensible sounds
- inappropriate words
- confused
- orientated
What is the diagnosis of the worst headache of life in the back of head, coming on very quickly in a couple of seconds?
Subarachnoid haemorrhage
What are the causes of sub arachnoid haemorrhage?
85% are from rupture of berry saccular (berry) aneurysms The rest are not due to aneurysms and may be due to: arterial dissection AV malformation tumour cocaine trauma septic aneurysm
Where are the common sites for berry aneurysms?
Junction of posterior communicating artery with the internal carotid.
Junction of the anterior communication artery with the anterior cerebral artery.
Bifurcation of the middle cerebral artery
What are the risk factors for berry aneurysms?
PKD, coaractation of aorta, Ehlers- Danons,
What investigations help diagnose SAH?
CT detects >90% in first 48hrs
If CT is -ve but still clinically suspicisous can do an LP at 12hrs and will have xanthochromia (yellow colour from break down of blood)
+ve for red blood cells in the LP does NOT confirm SAH as it could be due to a bloody tap.
How do you manage a SAH?
Referal to neuro surgery
Re examine neuro system often (GCS, pupils,)
Maintain cerebral pressure by keeping BP > 160mmHg
Nomodipine, a Ca channel antagonist, reduces vasopasm and decreases morbidity from the cerebral ischemia.
Surgery - coiling is better than clipping
What are the complications of SAH?
Rebleeding - occurs in 20% in the first few days
Cerebral ischemia - due to vasospasm and may cause permanent deficit
Hydrocephalus - due to blockage of the arachnoid granulations
Hyponatraemia - is common, but do not manage with fluid restriction.
Where is the blood coming from in a subdural haemorrhage?
Bleeding is usually from bridging veins between the cortex and the venous sinus.
The blood collects between the dura and the arachnoid layers.
What are the risk factors for a subdural haeorrhage?
Men Age Alcoholism Epilepsy Anti coagulant therapy Thrombocytopenia
Usually occurs after a minor fall
Describe the changes seen on CT after a subdural:
The bleeding forms a sickle shape
The blood begins being hyperdense compared to the brain tissue, then in 2-3 weeks it becomes isodense an then after 3 weeks it becomes hypodense
Mid line shift may be present, and eventually the brain may herniate due to increased ICP
What are the symptoms and signs of a subdural?
fluctuating level of consciousness, physical and intellectual slowing, sleepiness, headache, personality change, unsteadiness.
increases ICP, seizures, localising neuro symptoms occur late
What classically cause extra dural bleeds?
Hit to the head over the parietal area damages the middle meningeal artery
What are the changes on CT seen in an extra dural bleed?
Lens shaped haematoma, with a skull fracture and mid line shift
What are the symptoms and signs of a extra dural bleed?
Initial LOC then recovers, followed by increasing drowsiness (lucid period)
Increasing headache, vomiting, confusion and fits. hemipariesis and ipsilateral pupil dilatation.
BP rises and HR decreases - Cushings response to increasing ICP.
What is motor neurone disease?
A degenerative disease characterised by selective loss of neurones in the motor cortex, cranial n nuclei and anterior horn cells
Upper and lower motor neurones are affected but sensory cells are NEVER affected (helps to distinguish from MS and other polyneuropathies)
It NEVER affects eye movements (helps distinguish from myasthenia)
Fasiculations are very common!
What are the 4 different clinical patterns of MND?
Amyotrophic lateral sclerosis (classic MND)
Loss of motor neurones and anterior horn cells in spinal cord - causes weakness with UMN signs and LMN wasting
Progressive bulbar palsy
Only affects cranial nerves IX - XII. LMN lesions of the tongue and muscles of talking and swallowing: flaccid fasiculating tongue, quiet hoarse voice.
Often progresses to ALS
Progressive muscular atrophy
Anterior horn cell lesions only - no UMN signs.
Affects distal muscle groups before proximal
Primary lateral sclerosis
Loss of Betz cells in the motor cortex - mainly UMN signs.
Marked spastic leg weakness and pseudo bulbar palsy (UMN lesions of muscles of swallowing and talking, slow tongue movements, slow deliberate speech, increased jaw jerk)
How do you diagnosis ALS?
Clinical diagnosis - El Escorial diagnostic criteria
Definite = lower + upper motor neurone signs in 3 regions
Probable = lower + upper motor neurone signs in 2 regions
Probably with lab support = Lower + upper motor neurone sign in 1 region or UMN sign in >1 region + EMG shows acute denervation in >2 limbs
Possible = lower and upper motor neurone signs in 1 region
Suspected = upper or lower motor neurone sign in 1 or more regions
What is myasthenia gravis?
Autoimmune disorder - antibodies to nicotinic acetlycholine receptors, results in fewer receptors on the post synaptic membrane so fewer neuromuscular transmissions can occur.
What are the symptoms and signs of Myasthenia Gravis?
Increasing muscle fatigue - extraocular, bulbar, neck and shoulder girdle muscles are often affected first. Patients complain of double vision and ptsosis.
Tendon reflexes are normal
Anti AChr antibodies are raised in 90%
On repetative nerve stimulation a decremental muscle response is seen
If 50yrs more common in men and associated with thymic atrophy or thymic tumour.
How do you treat Myasthenia Gravis?
- Anticholinesterase (increases the amount of Ach around)
- Prednisolone for relapses - can use azathioprine and methatrexate of needed
- thymectomy
What are the differentials for generalised muscle weakness?
MND - fasciculations
Muscular dystrophies - can be selective weakness and FHx
Dystrophia myotonica - ptosis, wasting of masseter, temporal and SCM muscles. May be gondal atrophy, and mental retardation. FHx. EMG diagnostic
Polymyositis - acute or chonic, skin rash and joint pains
Miscellaneous - thyrotoxic, hypothyroid, cushing’s, alcoholic
Non metastatic associations of malignancy - thymoma, small cell lung cancer (Eaton - Lambert)
What are the causes of vertigo?
Peripheral (labyrinth and CVIII):
Benign positional vertigo -
due to debris in the semicircular canal
lasts for less than 1min at a time
occurs when moving head
Nystagmus on Hallpike manoeurve is diagnostic
the Eply manoeurve clears the debris
Vestibular neuronitis (acute labyrinthitis)
abrupt onset
N&V, no deafness or tinnitus
caused by viruses or vascular lesion
will settle on own
Meniere’s disease
endolymphatic hydrops causes recurrent attacks
each episode lasts >20mins
N&V, and tinnitus, and sensorineural hearing loss
Antihistamine can help
Ototoxicity
aminoglycosides, loop duiretics, cisplatin
Herpes zoster
Central - often have nystagmus Brainstem ischemia Posterior fossa tumours MS Alcohol/ drugs Migraine Epilepsy Acoustic neuroma - Schwannoma rises from the vestibular nerve. Unilateral hearing loss and vertigo. Ipsilateral V, VI, IX and X nerve involvement. VIII is not damaged until surgery
What are the red flags when patients complain of a headache?
Worsening headache with fever - meningitis
Sudden onset reaching max intensity in 5mins - SAH
New onset neurological deficit
New onset cognitive deficit
New change in personality
Impaired LOC
Recent trauma
Worse when coughing sneezeing laughing - high ICP
Headache triggered by exercise
Headache that changes with posture
Symptoms suggestive of GCA or Acute angle glaucoma
Different to normal headache