Neurology station Flashcards
stroke signs
Signs on inspection = circumducting gait, strong flexors in arms, strong extensors in legs, fixed flexed arm = pyramidal weakness, walking aids, wasted on affected side, increased tone/clonus, clasp knife spasticity, brisk reflexes and upgoing plantars
UMN signs
increased tone, increased reflexes, clonus, upgoing plantars contralateral
LMN signs
decreased tone, decreased reflexes, fasiculations, ipsilateral
pseudobulbar involvement
UMN Cranial nerves 9,10,12
Bulbar involvement
CN 9,10,11 = swallow and speech - aspiration and nutrition = PEG or NGT
LMN
What do you need to assess for in query stroke
Assess visual fields for Bamford classification
Assess pulse for AF and carotids for bruits.
how do you differentiate between bulbar vs pseudobulbar involvement
LMN would have fasciculations and wasting (bulbar)
stroke presentation
Today I performed a neurological examination on this gentleman. On general inspection he looked alert. He showed a circumducting gait on walking on the right with a flexed arm and extended leg. There was associated clasp knife spasticity, and hyperreflexia on the right. Clonus was present on the right, and plantars were upgoing. Power was 4/5 on the right. His left side was normal with power 5/5. These findings are consistent with a left sided partial anterior circulation infarct. I would like to take a full history, and feel his pulse for AF, listen to his carotids for bruits.
bamford classification
- TACS = total anterior circulation stroke = hemiplegia, homonymous hemianopia, higher cortical dysfunction
- PACS = partial anterior circulation stroke = 2/3 of above
- Lacunar stroke = hemi-motor or hemi-sensory stroke only
- Posterior circulation stroke = visual field defects
ACA
leg > arm
so may have fixed extended leg but normal arm
MCA
arm > leg
parkinsonism signs
Gait = shuffling, slow turn, asymmetrical limited arm swing
Face = expressionless, slow monotonous speech
Other = asymmetrical, pill rolling resting tremor, bradykinesia, rigidity, cogwheel rigidity
causes of parkinsonism
Idiopathic Parkinson’s disease
Lewy Body dementia (early dementia signs)
Multisystem atropy (if postural hypotension)
Supranuclear palsy (if palsy of eye movement)
Drug induced (if antipsychotics)
treatment of parkinsons
Conservative = carers, MDT, management of other comorbidities, optimising housing
Medical = Levodopa, co-carelodopa = reduced peripheral breakdown of dopa
Surgical = deep brain stimulation
Parkinsons presentation
Today I examined this gentleman’s neurological system. He was slow to start and slow to turn on walking. He had a shuffling gait with reduced arm swing on the left. He had a resting tremor in his left hand and there was marked rigidity on the left arm. Power and reflexes were normal. There was bradykinesia on examination of repeated movements. These findings are consistent with Parkinsonism. I would like to measure his lying and standing blood pressure, examine the eye movements, and perform an examination of his higher cognitive function to assess for the cause of his parkinsonism.
motor neurone disease signs
Mixed upper and lower motor signs
Fasciculations, increased tone, absent and brisk reflexes, upgoing plantars, bulbar or pseudobulbar tongue and speech
Normal sensory examination
motor neurone disease signs
Mixed upper and lower motor signs
Fasciculations, increased tone, absent and brisk reflexes, upgoing plantars, bulbar or pseudobulbar tongue and speech
Normal sensory examination
MND presentation
Today I examined this gentleman’s neurological system. He had reduced muscle bulk in all limbs and fasciculations. Tone was increased with brisk reflexes in the upper limbs but the knee and ankle jerk reflexes could not be elicited. Plantars were upgoing. There was globally reduced power in all limb at 4/5. Sensory examination was normal. These findings are consistent with a diagnosis of motor neuron disease. I would like to examine for bulbar involvement and take a full history.
DDx for mixed upper and lower signs
Motor neuron disease
Dual pathology e.g. peripheral neuropathy and stroke
Conus medullaris
B12 deficiency
Facial nerve palsy UMN
stroke = cerebral hemisphere lesion = contralateral + preservation of frontalis muscles FOREHEAD SPARED
Facial nerve palsy LMN
facial nerve lesion = ipsilateral and frontalis weakness = FOREHEAD AFFECTED
what is bells phenomenon
eyeball up and out to protect cornea
causes of facial nerve palsy
Stroke/MS = Pons = corticospinal tract signs
Acoustic neuroma = cerebello-pontine angle = 5, 6 , 7 palsies
Cholesteatoma = inner ear lesion = 8th nerve palsy
Parotid tumour = facial nerve = parotid scar/swelling
ramsey hunt syndrome
lyme disease
management of bells palsy
Prednisolone if <72 hours
Eye protection
Anti-virals not usually used
unilateral facial palsy
Herpes zoster – Ramsey Hunt
Diabetes mononeuropathy
Tumour
signs of MS
young, female. Catheter, walking aids, increased reflexes and tone, internuclear ophthalmoplegia, optic atrophy and RAPD
management of MS
MDT
Disease modifying drugs = interferon, alemtuzumab, natalizumab
Methylprednisone for flare ups
Baclofen for muscle spasms
cerebellar syndrome examination
- Gait = broad and unsteady, ataxia worse when heel-toe walk
- Arms = decreased tone, decreased reflexes, dysdiadokinesia, past pointing and intention tremor, rebound overshoot
- Eyes = nystagmus = cerebellar nystagmus = fast towards the lesion and worse towards affected side
- Speech = british constitution, west register street
DANISH
dysdiadokinesia
Ataxia
nystagmus
intention tremor
slurred speech
hyporeflexia, hypotonia
causes of cerebellar syndrome
Multiple sclerosis = young female
Stroke = older, AF, CABG, tar staining
Alcohol = liver disease
Phenytoin
what is Charcot Marie tooth disease and how to investigate
Muscle wasting
Thickened nerves
BL, symmetrical LMN foot drop, high step gait, absent ankle jerk
Stocking distribution loss of sensation
Ix via Nerve conduction studies and Genetic testing
Contralateral superior quadrantopia
temporal superior
Contralateral inferior quad
Parietal inferior
what is 3rd nerve palsy
Down and out
Ptosis
Dilate palsy
causes of 3rd nerve palsy
uncal herination
Cavernous sinus thrombosis,
PICA,
amyloid,
DM,
MS
horners
Ptosis, miosis, anhidrosis
horners causes
Stroke, sclerosis, tumour, carotid artery dissection
wernickes aphasia
receptive aphasia (temporal lobe) - comprehension is imparied
brocas apahsia
expressive aphasia (frontal lobe) - speech non fluent
Contralateral homonoymous hemianopia
optic tract
Bitemporal hemianopia
optic chiasm
LMN causes
polio,
lead poison
Alcoholic neuropathy
Leprosy
DM,
EToH
Vit b12 deficiency
causes of UMN
Abscess, cerebrovascular accident, tumour, demyelination, MS, cord compression, trauma, MND,
acute meningitis causes and treatment
Neonates = GBS, listeria, e.coli
Adults = s.pneumo, n.meningitidis
IV CEFTRIAZONE + IM BENZYLPENICILLIN
ELDERLY = + AMOXICILLIN
NEONATES = IV CEFOTAXIME + IV AMOXICILLIN
TIA treatment
Aspirin 300mg
Review by specialist
- Clopidogrel 75mg pO OD
- Statin
Surgery = carotid artery endarectomy
haemorrhagic stroke treatment
CT head if negative then LP with XANTHOCHROMIA
- Nimodipine CCB 21d
- First line = coiling
- Second line = surgical clipping
ischaemic stroke treatment
- Aspirin 300mg
- No AF = clopidogrel
- AF = apixaban
conductive hearing loss causes
Wax
Pus
Tympanic membrane perforation
Ossicle defects e.g. otosclerosis
sensorineural hearing loss causes
idiopathic
Drugs e.g. aminoglycosides or gentamicin
Infective = meningitis, measles, mumps
Meniere’s trauma, MS
Presbycusis - age related hearing loss
normal lower limb examination presentation
Today I performed a lower limb neurological examination of X year old Y.
On general inspection the patient was comfortable at rest, did not have any walking aids and had no bedside paraphernalia of neurological disease.
On closer inspection of the legs, the patient did not exhibit any stigmata of neurological disease such as scars or muscle wasting.
Tone was normal and no spasticity was noted.
Power was 5/5 in all muscle tested.
Reflexes, sensation, proprioception and coordination were normal in all modalities tested.
Gait was normal, and Romberg’s test was negative.
In conclusion this was a normal neurological examination of the lower limb.
To complete my examination, I would like to take full history and perform a cranial and upper limb examination.
I would like to take a full set of observations, perform a capillary blood glucose and take bloods, including FBC, U&Es and LFTs for baseline.
No further invasive tests are required at this point.
normal cranial nerve exam presentation
Today I performed a cranial nerve examination of X year old Y.
On general inspection the patient was comfortable at rest, did not have any walking aids and had no bedside paraphernalia of neurological disease.
On closer inspection of the face, the patient did not exhibit any stigmata of neurological disease such as face drooping or eye deviation.
Pupils were equal and reactive. There was no visual field abnormality and no pain on eye movement.
No abnormality was identified when testing cranial nerves 1 through 12.
In conclusion this was a normal neurological examination of the cranial nerves.
To complete my examination, I would like to take full history and perform an upper and lower limb examination.
I would like to take a full set of observations, perform otoscopy and fundoscopy exams, and take bloods, including FBC, U&Es and LFTs for baseline.
No further invasive tests are required at this point.
Normal upper limb examination presentation
Today I performed an upper limb neurological examination of X year old Y.
On general inspection the patient was comfortable at rest, did not have any walking aids and had no bedside paraphernalia of neurological disease.
On closer inspection of the arms, the patient did not exhibit any stigmata of neurological disease such as scars or muscle wasting.
Tone was normal and no spasticity was noted.
Power was 5/5 in all muscle tested.
Reflexes, sensation, proprioception and coordination were normal in all modalities tested.
There was not pronator drift or intention tremor noted.
In conclusion this was a normal neurological examination of the upper limb.
To complete my examination, I would like to take full history and perform a cranial and lower limb examination.
I would like to take a full set of observations, perform a capillary blood glucose and take bloods, including FBC, U&Es and LFTs for baseline.
No further invasive tests are required at this point.
drugs causing Parkinsonism’?
! Chlorpromazine
! Metoclopramide
! Prochlorperazine
! Sodium valproate
! Methyldopa
what is parkinsons disease
Parkinson’s disease is a neurodegenerative disease caused by disruption of dopaminergic
neurotransmission in the basal ganglia. The loss of dopaminergic neurones occurs most prominently
in the ventral lateral substantia nigra. Approximately 60–80% of dopaminergic neurons are lost
before the motor signs of Parkinson’s disease emerge.
what are parkinsons plus syndromes
Parkinson-Plus conditions are neurodegenerative conditions with Parkinsonian characteristics but
with additional features that distinguish them from idiopathic Parkinson’s disease. examples:
- Multiple systems atrophy
- Progressive supranuclear palsy
- Corticobasal degeneration
