NEUROLOGY Flashcards
What is hoovers sign
When is it used
What does it show
Test done to assess functional pattern of weakness.
Eg, if someone has L weak hamstrings, put your hand under L hamstrings when testing power of R quads. There is a reflex when R hip flexes, that L hip will extend. You should feel this. But when the muscle alone is tested it is weak. This is hoovers sign.
When attention is on the muscle it is weak but when it is not the muscle is normal.
It shows an inconsistent pattern of weakness - relatives to attention in task
What questions should you ask about regarding a functional seizure
Duration of event
Were their eyes open (organic) or closed
Rhythmic shaking or not
Post ictal confusion
What are the three features of Parkinson’s
Tremor - resting, poll pin
tone- hypertonia
Time- slow, bradykinesia, slow speech
What sits in meckels cave
Trigeminal ganglia
V2 maxilla
V3 mandibular
(V1) ophthalmic goes through cavernous sinus
Describe the vertebrae nerve roots of the cervical spine
Vertabrae- C1-7
1 atlas
2 axis
Nerve roots C1-8
Have spinal nerve that exits superiorly to C1, tf, at C7 have C8 nerve root below
What nerve roots make up the brachial plexus
C5-T1
Which cranial nerve enters and exits the cranial cavity
Where is it’s nuclei
What is it’s function
Enters foraman magnum
Exits jugular foremen with vagus
Nuclei from c1-c6
Function- sternocleidomastiod, traps
How is Lewy body dementia diagnosed
Onset of dementia within 2 years of Parkinson’s diagnosis (or onset)
After this it is Parkinson’s dementia
What diseases can mimic Parkinson’s
How do you assess for them
Progressive supranuclear palsy (upwards eye gaze) (build up of tau)
Cortico-basal degeneration (apraxia), akineasea one limb, involvement of sensory loss
Multiple system atrophy (autonomic features)
List some PD differentials
Parkinson’s Mimics (SNP, CBD) Vascular/ hypertension Parkinson’s (drugs can cause this as well, neuroleptic) Medications- antipsychotics Cerebellar disease Psychiatric conditions?
What is the typical presentation of Parkinson’s
What is atypical and what would this suggest
Typical is triad of Parkinsonism;
Resting tremor (asymmetrical)
Bradykinesia (facial, speech, tone, movements, getting dressed, ADL)
Hypertonia (rigidity, lead pipe, cogwheel = tremor + rigidity)
Atypical = some Parkinsonism but not triad. Features particularly in legs. ?vascular cause ?pressure hydrocephalus MRI to look for any spots of damage DAT scan
What is apraxia
What is a gait apraxia
Apraxia is difficulty planning a motor skills
Gait apraxia would be difficulty getting going and turning but ok once started
List some of the autonomic features of Parkinson’s
Explain why these occur
Increased secretions - saliva (drooling)
Because less dopamine - DA precursor to NA, so less NA for sympathetic NS, more parasympathetic
What monitoring is required for clozapine and why
ECG/ echo- myocarditis
Bloods - agranulocytosis
What is myesthenia gravis
What are the investigations
What is the management
Autoimmune disease, antibodies to the nicotinic acetylcholine receptor (AChR) on the post-synaptic membrane of neuromuscular junction
Bloods - look for autoantibodies
Electromyograph - decremental muscle response to repetitive nerve stimulation
CT to exclude thymoma
Acetylcholinesterase inhibitors Immunosupressants (steroids) IVIG Plasma exchange Sometimes thymectomy - even in pts who don't have a thymoma
What differentials would you consider in someone with fatigability
Myasthenia gravis
Polymyositis/ other myopathies
SLE
Takayasu’s arteritis
What should your examination include in a patient with myasthenia gravis
Look for ptosis
Get patient to gaze upwards for about 10 seconds - see if there is a ptosis (drooping/ falling eyelid)
Ask to flex shoulder joint 10x, see if they fatigue
What is the hallmark symptom of myasthenia gravis
Fatigable weakness - weakness that gets worse as the day goes on
Most commonly affecting the eyes (extraocular muscles), neck, upper limbs
What are the serious complications of myasthenia gravis
Slow breathing down
Always need to review respiratory rate in someone with MG
Type 2 respiratory failure
Where are nicotinic acetylcholine receptors
1.On skeletal muscle
Post-synaptic membrane
2.Autonomic ganglia - symp and parasymp - S/E, increased salivation, lacrimation, sweats, vomitting, miosis (excessive pupil constriction)
3. Nuclei in the brain
What conditions is MG associated with
Other autoimmune - Grave’s, RA, SLE
thymoma / thymic hyperplasia 85%
What is miosis
excessive constriction of the pupil
What are diplopia and ptosis signs of
Ocular weakness
How would you treat someone in myasthenia crisis
Plasmapheresis
Remove AChR antibodies from the circulation
List some postictal features
Postictal confusion
Postictal psychosis
What is a functional seizure
How would you explain this to a patient
It is a seizure where there is no organic pathology
It is a seizure that can happened whilst the brain is still normal and functional eg, there are no abnormalities found in any of the investigations or tests done.
Can explain this to patients using the example of the brain only having sensory information and learning as its tools to understand the world. When something makes these out of sync you can get seizures, but functionally the brain is still healthy and there is nothing to treat.
What can cause tunnel vision
Panic, stress, anger
Occular stroke, sudden drop in blood supply to brain
Papilledema
Glaucoma
What type of visual field defect would a posterior vascular event cause
Homonymous hemianopia
What neurological complications are there to heavy alcohol use
Wernickes (B1 deficiency) encephalopathy
Wernickes-Korsakoffs syndrome
Peripheral neuropathy
Hepatic encephalopathy (through liver cirrhosis)
Acute alcohol WD, seizures, psychosis
What investigation and examination would you do for hepatic encephalopathy
FBC, Haematinics, LFTs (GGT), U&Es
Ammonia (raised in hepatic encephalopathy) - can give something to help draw ammonia out in stool
Examine abdomen - distended? Ascites? fecal loading? Portal hypertensions signs? Jaundice?
What is the management of acute alcohol withdrawal
Chlordiazepoxide - benzodiazepine
Pabrinix - B and C vitamins, prevent wernickes
List some of the symptoms of alcohol withdrawal
Anxiety/Agitation/Irritability Nausea/Vomiting/Diarrhoea Convulsions Tremor of hands, tongue, eyelids Insomnia Hallucinations Sweating Fever with or without infection Delirium Tachycardia Hypertension
How do benzodiazepines work
Benzodiazepines enhance the effect of the neurotransmitter GABA at the GABAA receptor, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties.
How is the mechanism of action of alcohol
GABAa agonism
During withdrawal, inhibition via alcohol is gone and get overactivity causing seizures
What is an alternative to chlordiazepoxide in acute alcohol withdrawal
Lorazepam
Which part of the brain is damaged in wernickes encephalopathy
Brainstem and cerebellum.
Lesions are usually symmetrical in the periventricular region, diencephalon, the midbrain, hypothalamus, and cerebellar vermis. Brainstem lesions may include cranial nerve III, IV, VI and VIII nuclei, the medial thalamic nuclei, and the dorsal nucleus of the vagus nerve. Oedema may be found in the regions surrounding the third ventricle, and fourth ventricle, also appearing petechiae and small hemorrhages. Chronic cases can present the atrophy of the mammillary bodies.
What are the symptoms of wernickes encephalopathy
ophthalmoplegia
ataxia
confusion
Brainstem tegmentum. - Ocular: pupillary changes. Extraocular muscle palsy; gaze palsy: nystagmus.
Hypothalamus. Medulla: dorsal nuc. of vagus. - Autonomic dysfunct.: temperature; cardiocirculatory; respiratory.
Medulla: vestibular region. Cerebellum. - Ataxia.
What cells are granulocytes
Basophils
Eosinophils
Neutrophils
What are the features of an essential tremor
Bilateral With movement and testing (PD) tremor resting Subsides with distraction Functional signs
What is the management of an essential tremor
Propranolol if stress related
Haematinic supplements?
What is dystonia
What are the different causes / types
Painful muscle contractions
Primary - idiopathic (Botox)
Secondary- CP, MND, any condition of hypertonia, Parkinson’s
What bloods should you take in someone who has a ?essential tremor
TFT - hyperthyroid
U&E - K, NA, Mg
Blood sugars
What is
Akinesia
Dyskinesia
Bradykinesia
Akinesia - not moving
Dyskinesia - abnormal involuntary movements
Bradykinesia - slow voluntary movements
What questions should you ask in a pt with PD who is having difficulty with swallowing
Liquids or solids?
Any recent chest infections (? Aspiration)
What bloods should you check before starting biologics
TB, VZV, VDRL, HIV
Because it makes you immunosupressed
What investigations should you do for bilateral absent reflexes
Neuropathy bloods
What should you comment on during a gait exam
Posture Arm swing Stride length Turning Antalgic gait, ataxia, apraxia Feet - any foot drop, narrow or wide base
List some of the autonomic features of Parkinson’s
Why do they occur
Salivation
Increased parasympathetic secretions
Occur because of decreased dopamine = decreased NA, = decreased sympathetic innervation = increased parasympathetic drive
List some differentials for an unwitnessed loss of consciousness
Seizure - epilepsy vs functional
Syncope
Heart disease - arrhythmias
Space occupying lesion (?)
List some of the causes of encephalitis
Viral - HSV, CMV, VZV, HIV, MMR, tick borne
Non-viral - bacterial meningitis, TB, malaria, listeria, Lyme disease, legionella, leptospirosis, aspergillosis, crytpococcus, schisto, typhus
What are meningeal signs
Neck pain - brudzinskis sign
Kernigs sign
Photophobia - light sensitivity
Headache
List some non-infectious causes of encephalopathy
Hypoglycaemia Hepatic (high ammonia) Alcohol - wernickes acute, korsakoffs DKA Drugs Hyponatraenia (corrected too quickly) Hypoxia brain injury Uraemia SLE
What are the management options for MND
Riluzole - glutamate inhibitor and NMDA antagonist
Physio and OT
What are the feature of MND
Mixed upper and lower signs Eg, increased tone / rigidity and absent reflexes Fasiculations Pronator drift (lesion opposite side) Muscle wasting- look at thenar dorsum
How can you confirm brisk reflexes
Tap more gently
Then with fingers
Flick tip of finger- get reflex in thumb
Name the different types of lower motor neurone, what do they do
Alpha motor neuron- innervate motor unit (unit of contractile muscle fibres) - extrafusal
Gamma motor neuron- innervate intrafusal fibres- non contractile region / fibres that have stretch receptors in them
What are stretch receptors, what is their significance in disease
Receptions that monitor muscle length and velocity- when muscles stretches they connect with alpha and gamma MN- stimulate alpha MN to contract muscle
They are involved in maintaining muscle tone
Reflex is altered in diseases of pyrimadal and extrapyrimadal tracts
When innervation from UMN is depleted, stretch receptors are unopposed and get increased sensitivity and tone
When LMN is depleted, the sensitivity of stretch receptors doesn’t matter because Alpha MN is damaged and can’t stimulate muscle
What are the different possible causes for weakness
Cardiovascular event (aneurysm, stroke etc)
Inflammation (MS, encephalitis, infection)
Compression (tumour, meningioma etc)
Degeneration
How would you go about assessing the location of weakness
Find the level of lost function Cortical- focal paresis Internal capsule - hemiparesis Midbrain - bilateral paresis Spinal cord - bilateral paresis- evaluate level, anything below cervical spinal roots is legs only Nerve root LMN Neuromuscular junction Muscle
What are the possible brainstem causes of weakness
Inflammation - MS
Bulbar- MND
Infection - encephalitis
What test can you do to differentiate between cerebellar and vesribulocochlear ataxia
Unterbergers test (stepping test) Arms out eyes closed, stepping. Should do 50 steps. If rotate more than 30 degrees, indicates labrynth pathology on the side of turning
What is the unterberger test doing
The task is to hold arms out and to step with eyes closed
To do this, brain relies on the vestibulocochlear system for sense of balance
What structures lay in the cavernous sinus
Opthalmic division of trigeminal V1 Trochlear nerve Oculomotor nerve Maxilla V2 Carotids - internal Abducens Trochlear
What level does the cauda equina start
L2
What is the management of hepatic encephalopathy
Lactulose (increases ammonia excretion)
Rifaximin (reduces intestinal ammonia producing bacteria)
Enema
What would you see on a neuroshyphillis blood film
spherocytes (bacteria is a spherocyte)
What are the non infectious causes of encephalitis
Autoimmune
What part of the brain is associated with prosopagnosia
Fusiform gyrus- temporal lobe
What causes the sensation of dizziness in labrythitis
Movement of the endolymph in semi circular canals- even when not moving
What are the different types of MS
Relapsing remitting
Primary progressive
Secondary progressive
Progressive-relapsing
What are the features of secondary progressive MS
MS that started as relapsing and remitting but is now a steady decline, no remittance periods
What are the features of relapse and remitting MS
Attacks of disability, inbetween attacks disability does not decline
What are the features of progressive-relapsing MS
Steady decline in disability with periods where it is worse (an attack). No period where disease is static.
Where are the crus cerebri, what are they
In the midbrain - they are a continuation of descending motor tracts from the cortex
What is the vestibulo-ocular reflex
What is it’s significance
It is the reflex between the CN of the vestibular (head position) and the eyes. It’s function is to allow fixed gaze as the head moves, eg when you are walking, running etc, your eyes remain fixed so that vision is not erratic.
When someone has a vestibular problem (dizziness) can test this reflex to see if it is a problem with vestibular system or if it is central deficit
What is the head thrust test and when is it used
Its used to differentiate vestibular vs non-vestibular (CNS, cerebellar) pathology of dizziness.
Ask patient to look at your nose, hold their head and move 20 degree to their right.
If eyes maintain gaze on your nose, vestibular system in tact.
If there is a corrective gaze, look away with head movement and back at nose, suggests vestibular problem.
List the different vestibular tests you can do in examination
Head thrust Untenbergers test (stepping test)
What syndrome presents similarly to myasthenia gravis
What patients would get this
What are the autoantibodies
Lambert-Eaton syndrome
Patients with a pmhx of cancer
Autoantibodies against presynaptic calcium channels
What are the three symptoms of wernickes encephalopathy
Confusion
Opthalmoplegia (nystagmus, lateral palsy)
Ataxia
What are some causes for wernicks encephalopathy
Alcohol
Malnutrition
Anorexia
Severe D&V
What is Korsakoff’s syndrome
What areas of the brain are damaged
What are the symptoms
Damage to hypothalamic and cerebral areas- atrophy
Can’t form new memories, confabulation (retrograde amnesia), apathy
List a clinical approach to assessing weakness
Cortical (Focal weakness) Internal capsule (hemiparesis) Basal ganglia (extrapyramidal) Brainstem Spinal cord Anterior horn Nerve root Peripheral nerve (symmetrical and mono neuropathies) Neuromuscular junction Muscle
What differential should you consider in someone with ?PD
Wilson’s disease
Do bloods for caeruloplasmin
What is a cavernoma
Cluster of abnormal blood vessels, usually in the brain or spinal cord
What is the first line management of Huntington’s
Sulipride- D2 antagonist
Respiradrone
List some conditions that have Parkinsonism features but that are not PD
Dopamine antagonist medications- first and second gen antipsychotics, antiepileptics Other BG diseases: 1)PSNP 2)CBD 3)MSA 4)Lewy body dementia 5)Wilson’s disease - Cu deposited in BG
What is xanthochromia
Break down if RBC’s in the CSF
When would you see Kayser Fleisher rings
Wilsons disease
What are the symptoms of wilsons disease
Autosomal recessive
Liver disease signs
CNS signs - dysarthria, dysphagia,dyskinesias, dystonias
What is the definition of dementia
Neurodegenerative syndrome with progressive decline in several cognitive domains
What is delirium tremens
Acute confusional state caused by alcohol withdrawal
When does delirium tremens start
2-3 days of alcohol withdrawal
What is delirium
Acute confusional state with disorientation, difficulty communicating, reduced awareness, and changes in perception
