Neurology Flashcards
What does clasp knife spasicity suggest?
Pyramidal disease in upper motor neurone lesion
What does cog wheel rigidity suggest?
Extrapyramidal disease
Elicited by slowly pronating and supinating the patient’s wrist.
What is the muscle tested in shoulder ABduction?
Supraspinatus and Deltoid
What is the muscle tested in Shoulder ADduction?
Petoralis Major, Latissimus Dorsi
What is the muscle tested in Elbow Flexion?
Biceps and brachioradialis
What is the muscle tested in Elbow Extension?
Triceps
What is the muscle tested in Finger ABduction?
interossei
What is the muscle tested in Finger ADduction?
Interossei
What is the nerve root tested in shoulder ABduction?
C5
What is the nerve root tested in Shoulder ADduction?
Multiple, mainly C7
What is the nerve root tested in Elbow Flexion?
C5, C6
What is the nerve root tested in Elbow Extension?
C7
What is the nerve root tested in Wrist Flexion?
C7 and C8
What is the nerve root tested in Wrist Extension?
C7
What is the nerve root tested in finger ABduction and ADduction?
T1
What is the grading scale for power?
Medical Research Council Muscle Strength Scale
0: No visible Movements
1: Flicker of Movement on Active Contraction
2: Active movement with gravity eliminated
3: Active Movement against gravity but not against resistance
4: Active movement against gravity and resistance, but not normal strength
5: Normal
What does difficulty with past pointing and intention tremor suggest?
Cerebellar Disease
What does difficulty in dysdiadocokinesis suggest?
Cerebellar Disease
What are you testing in supinator reflex?
C5 & C6
What are you looking for in supinator reflex?
The contraction of the brachioradialis muscles- finger and elbow flexion
What are you testing in bicep reflex?
C5 & C6
What are you looking for in bicep reflex?
Contraction of the bicep muscles
What are you testing in triceps reflex?
C7
What are you looking for in triceps reflex?
Contraction of the tricep muscle
Where do you test dermatomes?
Picture
What nerve tract are you testing with proprioception?
Dorsal Column
What tuning fork in Neuro vibration sense?
128-Hz
What sensory modality are you testing with tuning fork?
Vibration- Dorsal Column
What is the muscle tested in Hip Flexion?
Iliosoas
What is the muscle tested in Hip extension?
Gluteus Maximus
What is the muscle tested in Knee Flexion?
Hamstrings
What is the muscle tested in Knee Extension?
Quadriceps
What is the nerve root tested in Hip Flexion?
L1 & L2
What is the nerve root tested in Hip Extension?
L5 & S1
What is the nerve root tested in Knee Flexion?
L5 & S1
What is the nerve root tested in Knee Extension?
L3 & L4
What is the muscle tested in Dorsiflexion?
Tibialis Anterior
What is the muscle tested in Plantar flexion?
Calf Muscles
What is the nerve root tested in Dorsiflexion?
L4 & L5
What is the nerve root tested in Plantar Flexion?
S1
Where do you assess Sensation on lower limb?
PIC
What are you testing in knee reflex?
L3 & L4
What are you looking for in knee reflex?
Knee Extension and quadricep muscle contraction
What are you testing in Ankle reflex?
L5 &S1
What are you looking for in ankle reflex?
Plantar flexion and contraction of the calf muslce.
What is a normal Babinski response?
Down going plantars.
What does the inability to tandem walk suggest?
Cerebellar disease
What does Romberg’s Test test for?
Sensory Ataxia
What are reflexes?
Monosynaptic responses to muscle fibre stretch, mediated via the spinal cord with inhibitary input from higher neurones.
In UMN lesions the inhibitory input from higher neurones is reduced and so reflexes are increased.
Pattern of Signs in an UMN lesion
Tone- Increased tone or spasticity, clonus
Power- Reduced: Mainly in arm extensors and leg flexors
Pronator Drift
Reflexes: Hyperreflexia
Inspection: No muscle wasting or fasiculaitons
Difference between Tone and Spasticity.
Spasticity is velocity dependent: tone decreases with velocity
Where is the lesion in an UMN relative to the signs?
Contralateral Side
Pattern of Signs in an LMN lesion
Tone: Hypotonia
Power: Reduced
Reflexes: Diminished/ Absent
Inspection: Muscle Wasting and fasiculaitons
Where is the lesion in an LMN relative to the signs?
Ipsilateral side
Differentials for UMN lesions
Stroke, MS
DDx for LMN lesions
Radiculopathy, Peripheral Neuropathy, Mononeuropathies
Features of Cerebellar Disease
Dysdiadokinesia Ataxia and Hypotonia Horizontal Nystagmus Intention Tremor with Pass Pointing Staccato or Slurred Speech Heel Shin Ataxia Wide based, unsteady ataxic gait- pt falls to side of lesion
How do you assess whether a tremor is an action tremor or not?
Rule out any muscle activation
Take the pts arms and support them in your arms.
A truley cerebellar tremor will disappear.
What are the causes of cerebellar disease?
- Space Occupying Lesions ( Tumours, Abcescess, Bleeds)
- Multiple Sclerosis
- Chronic Alcohol Abuse
- Anti- Epileptic Drugs e.g Phenytoin
What is the speed of a Parkinsonian Tremor?
4-7Hz
What happens in Parkinsons to Speech and Handwritin?
There is a slowing down of speech and micrographia
What is the extrapyramidal system?
The basal ganglia and it’s connections; especially those to do with movement.
The extrapyramidal system is charged with modulation and initiation of movement.
What is Parkinson’s Disease?
Progressinve Neurodegenerative disorder characterised by Lewy Bodies, neuronal loss and degeneration of the substantia nigra
Diagnosis is clinical, but some patients have L-Dopa or apomorphine challenges.
PET of MRI scanning is sometimes done to exclude other diagnoses
Causes of Parkinsonism
Parkinson’s Disease: Idiopathic
Treatment of Parkinson
…
How do you demonstrate Fatuigability in myasthenia Gravis?
Ask the patient to gaze upwards for a few minutes.
Pts with MG will get increased Ptosis
How would you complete your exam in a patient with suspected myasthenia gravis?
- Look for Thymectomy Scar
- Assess for signs of other AI disease
- Assess speech (get dyarthria and poor swallowing due to weak bulbar muscles)
- Check eyes: Get Ophthalmoplegia, ptosis and diplopia due to weak eye muscles.
How do pts with Myasthenia Gravis tend to present?
With diplopia, typically worse when tired.
How do you diagnose Myasthenia Gravis?
Clinical Diagnosis
Can use tensolin test. Give edrophonium (short active ACh) and get a rapid improvement in symptoms
What specialist investigations do you do for Myasthenia Gravis?
BLood test: Anti-Ach Antibodies
Tensolin Test
EMG- reduced amplitude of evoked potentials with repetative stimulation
What is Myasthenia Gravis?
Auto Immune disorder affective the neuromuscular junction. Antibodies block the action of post-synaptic acetylcholine receptors
What do you need to distinguish Myasthenia Gravis from?
Lambert-Eaton Syndrome
- Occular and bulbar muscles are not affected
- Second wind phenonemon
How do you treat Myasthenia Gravis?
Medical: Cholinesterase Inhibitors, Immunosuppressants and corticosteroids (But be careful as pts are at risk of myasthenia crises if there is a coexisting infection-some crises are drug induced)
Surgical: Thymectomy for Thymomas
Typical Examination Findings for Multiple Sclerosis.
UMN: Increased tone, Clonus, Brisk Reflexes, Weakness.. Bilateral.
Neuro-opthalmology:
Internuclear Ophthalmoplegia
Optic Nerve Damage
Cerebellar Signs: Ataxia, Dysarthria
Cranial Nerve Palsy: Facial Nerve
Sensation altered in a variable fashion. Altered temperature sensation, Trigeminal neuralgia, Lhermitts phenomenon-electric shock sensation down arms and legs on neck flexion.
May have catheter-neurogenic bladder dysfunction
DDx in pt with suspected MS
Spinal Cord LEsion: Tumour or trauma causing spastic paraparesis
Investigating Multiple Sclerosis
MRI Brian and Spinal Cord: First line investigation, reveals plaques or multiple white matter lesions, particularly in the brainstem and periventricular areas.
Electrophysiology: Prolonged Visual Evoked Potentials
CSF: High Protein, Raised WCC, Electrophoresis shows oligoclonal bands.
What is Multiple Sclerosis?
Neurological Disorder of unknown cause resulting in multiple areas of plaques of demyelination in the brain and spinal cord, disseminated in time and space.
There is a female predominance.
Characteristically begins in early adult hood: Clinical course can be broadly broken down to progressive and relapsing remitting.
What factors give poor prognosis in MS?
Male
Increased Age
Motor Symptoms
High Number of Relapses with incomplete remissions
How would you treat MS
This patient will require an MDT approach
The focus of the treatment is to prevent disability and its progression.
High dose steroids: Aid recovery and promote remission during acute relapses but do not affect long term prognosis
Beta-Interferon has been shown to delay progress of disability, reduce relapse rates and reduce disease activity.
Urinary catheteriastion- neurogenic bladder dysfunction.
Physio and OT- aid mobility and limit disability.
Muscle relaxants: Baclofen for painful spasticity
Pt and Family Self Help group referral
4 Groups of Cranial Nerves
- Olfactory
- Ophthalmology: II, III, IV, VI
- Cerebellopontine Angle Nerves: V, VII, VIII
- Bulbar Nerves: IX, X, XI, XII
What is a turned out eyelid called?
Ectropion
What is a turned in eyelid called?
Entropion
Causes of Entropion
- Congenital
- Age related
- Infection
- Trauma
Causes of Ectropion
Normally the Lower Lid
Styes (Hordeolum)- acute focal infection, usually staphyloccocal involving the glands of Zeis or meibomian glands
SE of Entropion
Redness and irritation due to inversion of eyelashes with excessive lacrimation
SE of ectropion
Corneal Exposure, lacrimation, scarring of the conjunctiva and eventually vision loss.
What is the causes of proptosis?
Increased volume in the fixed volume orbital cavity forcing the orbit forward
What are the causes of proptosis?
- Inflammatory
- Infection
- Vascular pathology
In Graves disease: AI reaction in orbital tissues which become infiltrated with inflammatory tissue and matter
What does iritis look like?
Mudded iris, often with pupil constriction
When do pupils constrict?
- Light
- Extremes in age: Old and infancy
- Sleep
When do pupils dilate?
- Fear
- Excitement
- Poor light
What happens in the accommodation reflex
Pupils constrict and converge
Pathological cause of a Small Pupil.
Miosis
- Argyll Robinson
- Horner’s Syndrome
- Iritis
Argyll Robinson pupil
Small, irregular pupil.
Doesn’t react to light but accommodates
Horner’s Syndrome
Miosis
Ptosos
Anhydrosis on affected side
Due to lesion in the sympathetic chain.
Pupil reacts normally to light and accommodation
Iritis
Poor reaction to light and accommodation
Pathological cause of large pupil (Mydriasis)
- Holmes-Aidie Pupil
2. 3rd Nerve Palsy
Holes-Adie Pupil
Congenital, Slow, incomplete reaction to light. Accommodation is slow/ Normal.
Holmes Adie Syndrome if loss of deep tendon reflexes
CN3 Lesion
Interruption of parasympathetic chain, no reaction to light or accommodation. BUT normal side still reacts consensually
Aeitiology of Arcuate Scotoma
Glaucoma
Aeitiology of Central Scotoma
Macular Degeneration
Aeitiology of Unilateral Deficit
PIC
Arterial Occulsion
Branch Retinal Vein Occlusion
Retinal Detachment
Superior Homonomous L/R sided quadrantinopia
Right sided means left temporal lesion
Inferior Homonomous L/R sided quadrantinopia
Right sided means left parietal lesion
Homonomous Hemianopia
Right field deffect means Left OPtic radiation or visual cortex
Bitemporal hemianopia
Lesion a optic Chiasm
Loss of vision in one eye
Optic nerve lesion
Complicated lesion of Chiasm
What are the branches of the Facial Nerve?
To Zanzibar by Motor Car
Temporal, Zygomatic, Buccal, Marginal Mandibular, Cervical
Causes of facial nerve palsy
- Bells Palsy
- Infective: Ramsay Hunt Syndrome, Lyme Disease, TB
- Brain Lesons: in brainstem and cerebellopontine angle
- Others: ENT, Trauma, etc
- Bells Palsy: Classically described as idiopathic but can be viral. Typically Facial Weakness is the only sign.
- Ramsay-Hunt Syndrome: Reactivation of Herpes Zoster in the geniculate ganglion–> altered taste and vesicles in the external auditory meatus
- Brainstem= Tumours, MS, CVA
- Cerebellopontine Angle= Meningioma, Acoustic Neuromas
- ENT: Otitis Media, Cholesteatoma, Parotid Tumours
- Trauma: Base of skull fracture, barotrauma whilst diving
others include: DM, Guillain-Barre Syndrome
What is Bells Phenomenon?
On attempted closure of the eye the eye rolls up
It is due to weak orbicularis oculi muscles resulting in difficulty in closing eyes
Key features of Bells Palsy
Unilateral- Facial Droop Bells Phenomenon: Weak Orbicularis Oculi Inability to raise eyebrow: Weak frontalis muscle Inability to frown Smooth Nasolabial Fold
How do you localise a facial nerve palsy
- Ask about changes in hearing- Hyperacusis suggests lesion distal to the stapedius branch
- Ask about changes in lacrimaiton and taste- Major branch of facial nerve, Chorda Tympani goes through facial canal of petrous temporal bone.
Treatment of Bells Palsy
Steroids- within 6 days
? Aciclovir
Eye protection