Neurology Flashcards
Describe neurofibromatosis, it’s types, and features and diagnosis.
There are two types NF1 and NF2 both are automsomal dominant.
NF1 features with cafe-au-lait spots, axillary/groin freckles, peripheral neurofibromas, iris hamartomas, scoliosis, phaeochromocytomas.
NF2 features with bilateral acoustic neuromas.
Diagnosis of NF1 assessed by seven clinical criteria at least two of which should be present:
- Six or more Cafe-au-lait spots or hyper pigmented macules greater than of equal to 5mm in diameters in pre-pubertal individuals and 15mm in post-pubertal individuals.
- Two or more neurofibromas or one plexiform neurofibroma
- Axillary of inguinal freckles
- Two or more iris hamartomas (Lisch nodules), often identified only thought slit-lamp examination by an ophthalmologist
- optic nerve glioma
- Sphenoid dysplasia or typical long-bone abnormalities such as psuedouarthrosis
- First-degree relative with NF1.
What are the features of a UMN lesion?
Affects muscle groups Upgoing plantar reflex (+ve babinski)/clonus Hyperreflexia No fasciculations Spasticity/hypertonia
What are the featured of a LMN lesion?
Caused by damage from anterior horn cells, nerve roots, plexi, or peripheral nerves
Wasting and fasciculations
Hyporeflexia
Downward going plantars (-ve babinski)
Hypotonia (flaccidity)
What does the anterior cerebral artery supply and what symptoms arise from its occlusion?
Supplies the frontal and medial part of the cerebrum.
Occlusion may cause a weak,numb contralateral leg +/- similar but often milder picture in the arms. The face is spared.
What does the middle cerebral artery supply and what symptoms arise from its occlusion?
Supplies the lateral part of each hemisphere
Occlusion may cause a weak contralateral hemiparesis, Hemisensory loss (esp arm + face), contralateral homonymous hemianopia.
What does the posterior cerebral artery supply and what symptoms arise from its occlusion?
Supplies occipital lobe
Occlusion gives contralateral homonymous hemianopia (often with macular sparing)
Describe subclavian steal syndrome
Subclavian artery stenosis proximal to the origin of the vertebral artery may cause blood to be stolen by retrograde flow down this vertebral artery down into the arm, causing brain stem ischaemia typically after use of the arm.
Suspect if the BP in each arm differs by >20mmHg
What are some causes of an acute single episode headache?
- With meningism: meningitis, encephalitis, subarachnoid haemorrhage
- Head injury
- Venous sinus thrombosis
- Sinusitis
- Tropical illness
- Low pressure headache
- Acute glaucoma
What are some causes of recurrent acute attacks of headache?
- migraine
- cluster headache
- trigeminal neuralgia
- recurrent (mollaret’s) meningitis
What are some causes of subacute onset headaches?
Giant cell arteritis should be excluded in all >50yrs old with a headache that has lasted a few weeks.
What are some causes of chronic headache?
- Tension Headache
- raised ICP
- Medication overuse (analgesic rebound) headache
Describe tension headache, its symptoms, and management
Symptoms:
Usual cause of bilateral, non pulsating headache +/- scalp tenderness, but without vomiting or sensitivity to head movement.
Management:
- Stress relief, massage, or antidepressant (low dose amitryptilline) may help.
- Consider seeing optician
Describe raised intracranial pressure, its symptoms and tests.
Symptoms:
Typically worse on waking, lying, bending forward, or coughing. Also vomiting, papilloedema, seizure, false-localising signs, or odd behaviour
Tests: Do imaging to exclude a space-occupying lesion, and consider idiopathic intracranial hypertension. LP is contraindicated until after imaging!
Describe Acute Glaucoma, it’s presentation, symptoms, and management.
Presentation: Typically elderly, long-sighted people. Constant, aching pain develops rapidly around one eye, radiating to the forehead. Attacks may be precipitated by dilating eye-drops, emotional upset or sitting in the dark.
Symptoms: markedly reduced vision, visual haloes, nausea/vomiting.
Signs: red congested eye, cloudy cornea, fixed dilated non-responsive pupil (may be oval), decreased acuity.
Management:
seek expert help, if delay of treatment of >1h start acetazolamide 500mg IV over several minutes.
Describe Cluster Headaches, its features, and management
Unilateral severe headache that occurs once or twice a day for 15-180mins and is often nocturnal, usually lasting several weeks, with the clusters themselves occuring typically once a year. Clusters may be episodic or chronic. 5 times more common in men, can occur at any age and more common in smokers.
Features:
-Rapid-onset of excruciating stabbing pain around one eye that may become watery and bloodshot with lid swelling, lacrimation, facial flushing, rhinorrhoea, miosis+/- ptosis.
Management:
- acute attack: 100% O2 (80% response rate within 15 minutes) + Sumatriptan SC 6mg (75% response rate within 15 minutes)
- Prophylaxis: Verapamil is the drug of choice, some evidence supports a tapering dose of prednisolone
- Neurology referral
Describe epilepsy and its suggestive features.
Epilepsy is a recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures.
Features suggestive of epilepsy: attacks when asleep or lying down, aura, identifiable triggers (e.g. tv) altered breathing, cyanosis, typical tonic-clonic movements, incontinence, tongue-biting, prolonged post-ictal drowsiness (slow recovery), confusion, amnesia, and transient focal paralysis (Todd’s palsy)
What are some causes of seizures?
- Idiopathic ~ 2/3
- Structural: (cortical scaring, developlmental, space-occupying lesion, stroke, hippocampal sclerosis, vascular malformations)
- Others: tuberous sclerosis, sarcoidosis, SLE, PAN
- Non-epileptic causes: trauma, stroke, haemorrhage, increased ICP, alcohol or benzodiazepine withdrawal, metabolic disturbance (e.g. hypoxia, hypo/hypernatraemia, hypocalcaemia, hypo/hyperglycaemia, uraemia) liver disease, infection, hyperthermia, drugs (tricyclics, cocaine, tramadol, theophylline), pseudoseizures.
What are the classifications of seizures?
The basic classification of epilepsy has changed in recent years. The new basic seizure classification is based on 3 key features:
- where seizure begin in the brain
- level of awareness during a seizure
- other features of seizures
Focal seizures:
- previously termed partial seizures
- these start in specific area, on one side of the Brain.
- the level of awareness can vary, the terms focal aware (previously simple partial) or focal awareness impaired (previously complex partial) and awareness unknown are used to further differentiate focal seizures
- Further to this focal seizures can be classified as being motor (e.g. Jacksonian march), non-motor ( e.g. dejavu, jamais vu). or having other features such as aura.
Generalised seizures:
- these engage or involve networks job both sides of the brain at onset.
- Consciousness is lost immediately.
- Generalised seizures can be further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence)
- specific types include, tonic-clonic, tonic, clonic, absence, myoclonic, atonic.
Unknown onset: a term reserved for when origin of the seizure is unknown.
Focal to bilateral:
- starts on one side in a specific area before spreading to both lobes
- previously termed secondary generalised seizures.
Define a focal aware seizure
Awareness is unimpaired. with focal motor, sensory, autonomic or psychic symptoms. no post-ictal symptoms.
Define a focal impaired awareness seizure
awareness is impaired. may have a simple partial onset or impaired awareness at onset. most commonly arise from the temporal lobe. Post-ictal confusion is common with seizure arising from the temporal lobe, whereas recovery is rapid after seizures in the frontal lobe.
Define a focal to bilateral seizure
occurs in ~ 2/3 of patients with partial seziures, electrical disturbances begin focally as either complex or simple seizures but then spread widely, causing a secondary generalised seizure which is typically convulsive.
Describe Absence seizures, and its management
Brief (less than 10s) pauses, e,g, suddenly stops talking mid-sentence then continues where they left off. Presents in childhood 4-8yrs.
Management:
- Sodium Valproate, Ethosuximide
- Good prognosis 90-95% become seizure free in adolescence.
Define tonic-clonic seizures
loss of consciousness. limbs stiffen (tonic), the jerk (clonic) may have one without the other. post-ictal confusions and drowsiness occur.
Define myoclonic seizures
sudden jerk of a limb, face of trunk. the patient may be thrown suddenly to the ground or have a violently disobedient limb.
Describe atonic (akinetic) seizures
sudden loss of muscle tone causing a fall, no loss of consciousness
What are some localising features of partial focal temporal lobe seizures?
- Automatisms (brief complex motor phenoma with impaired awareness/ no recollection e.g. may be oral or manual.
- abdominal rising sensation +/- pain
- dysphasia
- memory phenonema e.g. dejavu or the opposite jamais vu
- hippocampal involvement may cause emotional disturbance e.g. terror, anger
- Uncal involvement may cause hallucinations fo smell or taste
- Auditory hallucinations
- delusional behaviour
What are some localising features of partial focal frontal lobe seizures?
- Motor features
- motor arrest
- subtle behavioural distubances
- dysphasia or speech arrest
- post-ictal todd’s palsy
What are some localising features of partial focal parietal lobe seizures?
- sensory disturbances
- motor symptoms
What are some localising features of partial focal occipital lobe seizures?
visual phenomena such as spots lines or flashes
Define pseudo- or psychogenic seizures
these are not infrequent suspect if there are uncontrollable symptoms, no learning disabilities, and CNS, CT, MRI and EEG are all normal. May be part of Munchausen’s syndrome
What are the drug used in treatment of epilepsy?
Generalised tonic-clonic seizures - sodium valproate or lamotrigine are 1st line, then carbamazepine or topiramate.
Absence seizures - ethosuximide, sodium valproate, lamotrigine.
Tonic, atonic, and myoclonic seizures same as tonic-clonic but no carbamazepine as it may worsen seizures.
Focal seizures - carbamazepine is first line then lamotrigine and valproate
What are the side effects of sodium valproate
V alproate side effects A ppetite increased leading to weight gain L iver failure (LFT monitoring) P ancreatitis R eversible hair loss (grows back curly) O edema A taxia T eratogenicity, tremor, thrombocytopenia (Monitor bloods) E ncephalopathy
How do you assess risk of stroke in patients presenting with TIA?
ABCD2 score - >6 strongly predicts stoke, >4 should be assed within 24 hours all suspected TIA should be seen within 7 days.
A ge>60 = 1 point
B lood pressure >140/90 = 1 point
C linical features
unilateral weakness = 2 points
speech disturbance without weakness = 1 point
D uration of symptoms
lasting > 1h = 2 points
lasting 10-59 mins = 1 point
D iabetes = 1 point
Describe Cauda equina syndrome and its symptoms.
A neurosurgical emergency!
Symptoms: Features include back pain and radicular pain down the legs, assymetrical (alternating or bilateral), atrophic, areflexic paralysis of the legs. Sensory loss in a root distribution (saddle anaesthesia) and decreased sphincter tone causing bladder and bowel incontinence (Do PR)
What would you expect to see on CSF analysis from LP of suspected bacterial meningitis?
Appearance: cloudy
Glucose: low less than half plasma glucose
Protein: high >1g/L
White cells: 10-5000 polymorphs/mm
What would you expect to see on CSF analysis from LP of suspected tuberculous meningitis?
Appearance: slightly cloudy, fibrin web
Glucose: low less than half plasma glucose
Protein: high >1g/L
White cells: 10-1000 lymphocytes/mm
What would you expect to see on CSF analysis from LP of suspected viral meningitis?
Appearance: clear/cloudy
Glucose: 60-80% plasma glucose
Protein: normal/raised
White cells: 15-1000 lymphocytes/mm
What are the main features of Parkinsonism?
- Tremor (worst at rest, often ‘pill-rolling’)
- bradykinesia (diagnostic feature)
- rigidity/ increased tone (tremor + rigidity gives cogwheel rigidity felt during pronation and supination of arm)
What are some causes of Parkinsonism?
- idiopathic Parkinson’s,
- drug induced (anti-psychotics and anti emetics (domperidone does not cross the blood brain barrier)
- Progressie supranuclear palsy
- Multiple system atrophy
- Dementia Pugilistica (secondary to trauma/boxing)
- Wilson’s disease
- Post-encephalitis
- HIV
- vascular
- Toxins e.g. Carbon monoxide, MPTP
Describe idiopathic Parkinson’s disease, it’s presentation, and management..
Incurable progressive disease characterised by degeneration of neurones in the substantia Nigra pars compacta associated with lewy bodies which leads to a reduction in striatal-like dopamine
Presentation: bradykinesia + one or more of: resting tremor, postural instability, rigidity. Typically one side is worst often right side. Also micrographia, depression, decreased cognition (Lewy body dementia), slow festinating gait, simian posture,
Management: levodopa, dopamine agonists (ropinirole), anticholinergics, MAO-B inhibitors (selegiline), COMT inhibitors (entacapone)
What are some causes of nystagmus?
- horizontal nystagmus may be due to vestibular or cerebellum lesions. If it occurs more in the eye abducting cause may be MS. If also deafness and tinnitus may be peripheral cause e.g. VIIIth nerve lesion
- vertical nystagmus requires specialist review, upbeat nystagmus classically occurs in lesions of midbrain or base of 4th ventricle. Downbeat nystagmus in foramen magnum lesions.
What are the symptoms of a cerebellum lesion?
D ysdiadokokinesis and dysmetria A taxia S lurred speech/stoccato speech H ypotonia I ntention tremor N ystagmus G ait abnormality
Describe Rhomberg’s test and meaning of its results
Rhomberg’s test is used to assess a patient proprioception when standing with their eyes closed. A loss of balance is a positive test
In the context of ataxia a patient with a positive Rhomberg’s suggest the ataxia is sensory in nature if it is negative it suggest the ataxia is of cerebellum origin
Describe subarachnoid haemorrhage, its symptoms, and management, and complications
80% are due to rupture of saccular aneurysms. Common sites for berry aneurysms are the junction of posterior communicating artery with the internal carotid (may present with pupil changes indicating a IIIrd nerve palsy) or the junction of anterior communicating artery with the anterior cerebral artery or bifurcation of the middle cerebral artery.
Symptoms: Usually presents with sudden onset devastating occipital headache, vomiting, collapse,seizures and coma often follow. May report a sentinel headache. Signs include Kernigs sign, neck stiffness.
Management:
- Do CT within 4 hours of presentation and if positive refer to neurosurgeons for endovascular coiling or less preferred clipping.
- If CT negative and no contraindications do LP 12 hours after presentation. Xanthachromia confirms Subarachnoid haemorrhage.
- Maintain BP and nimodipine to reduce vasospasm.
Complications:
- Hydrocephalus (occurs a few days after)
- Raised Intracranial pressure
- Rebleeding (Occurs in first 1-2 days or after 2 weeks)
- Delayed Ischaemia (Occurs around day 10)
What is Kernig’s sign?
Kernig’s sign is a positive when the hip is flexed to 90 degrees and there is paining resistance of extension of the knee. It is indicative of subarachnoid haemorrhage or meningitis
What is battle’s sign?
Bruising of the mastoid process a sign of basal skull fracture
What is Panda or Raccoon eyes a sign of?
It is bruising of the eyes a sign of basal skull fracture
Describe IIIrd Cranial Nerve palsy and its causes
Ptosis, large pupil, eye down and out.
If lesion present on it own causes may be:
- Medical (pupil sparing) e.g. Diabetes, HTN, GCA, syphillis idiopathic.
- Surgical (early pupil involvement) e.g. posterior communicating artery aneurysm, Increased ICP, tumours.
Describe IVth Cranial Nerve palsy and its causes.
Diplopia on looking down and in (often noticed on descending stairs) head tilting compensates for this (ocular torticollis).
Lesion rarely occurs on its own but possible after trauma to orbit. More commonly presents with other lesions.
Describe VIth Cranial Nerve palsy and possible causes.
The Abducens nerve. Horizontal diplopia on abduction.
False localising sign due to long intracranial course in Raised ICP, SOL,
Describe acoustic neuroma and its presentation, investigations, and management
It is a schwannoma arising from the vestibular nerve. They account for 80% of cerebello-pontine angle tumours. Commoner in females and also in neurofibromatosis.
Presentation: progressive unilateral tinnitus +/- sensorineural hearing loss, with vertigo occuring later. With progresion, ipsilateral Vth,VIIth, VIIIth, (IXth, Xth nerves may be affected later). Signs of increased ICP occur late, indicating a large tumour.
Investigations: MRI in all with unilateral tinnitus and deafness
Management: Surgery
Describe the red flags present in parkinson’s-plus syndrome
- Early postural instability and vertical gaze palsy +/- falls, rigidity of trunk > in limbs, symmetrical onset, speech and swallowing problems, little tremor = Progressive Supranuclear Palsy (PSP)
- Early autonomic features e.g. impotence/incontinence, postural BP drop, cerebellar + pyrimidal signs, rigidity>tremor = Multiple System Atrophy (MSA)
- Fluctuating cognition with visual hallucinations and early dementia = lewy-body dementia
- akinetic rigidity involving one limn and cortical sensory loss e.g. astereognosis (inability to recognise objects by touch alone) = cortico-basal degeneration
- Pyramidal signs e.g. in a diabetic/hypertensive patient who falls or has gait problems with no festination = vascular parkinsonism
Describe the pull test
a sharp tug on the back of a patients shoulders to test for postural instability a positive result is one in which a patient is unable to correct there balance and continues falling backwards after the tug.
What are some causes of cerebellar syndrome?
Posterior Fossa Tumour Alcohol Sclerosis (Multiple) Trauma Rare e.g. Iithium Inherited - Friedrich's ataxia Epilepsy medications e.g. Phenytoin, carbamazepine Stroke
Describe hemispatial neglect (hemiagnosia)
Damage to one hemisphere of the brain leads to a deficit in attention to and awareness of one side of observed space. It is usually contralateral to the lesion. Usually due to a lesion of the parietal cortex but in particular neglect is closely related to damage of the temporo-parietal junction and posterior parietal cortex.
Describe Visual extinction
Due to damage to the parietal lobe, similar but distinct from hemispatial neglect (hemiagnosia). Visual extinction describes the symptom in which patients have difficulty perceive contralesional stimuli e.g. moving fingers, when presented simultaneously wth an ipsilesional stimulus; but able to identify both stimuli when presented individually.
What is the difference between spasticity and rigidity
Spasticity is velocity dependant the initial fast movement is resisted and then gives way, usually uni-directional whereas rigidity is independent of velocity and is bidirectional.
Describe lateral medullary syndrome
Occurs after occlusion of most commonly the vertebral artery but also posterior inferior cerebellar artery.
Present with:
- cerebellar features e.g. ataxia, nystagmus
- brainstem features e.g. ipsilateral dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s and contralateral limb sensory loss
Describe Dysarthria
Dysarthria is a disorder of speech due to disturbance of muscular control. Can be caused by UMN lesions of the cerebral hemisphere or LMN of the brain stem.
There may be some variation depending on the site of the lesion:
- slurred and weak articulation with a weak voice is typical of pseudobulbar palsy from a stroke.
- slurred, scanning and staccato speech caused by cerebellar lesions is typical of MS.
- Dysrhythmic, dysphonic, monotonous voice can be due to disease of the extrapyramidal system in Parkinson’s.
Describe dysphasia
Dysphasia is impaired ability to understand or use language.it is due to a lesion of the dominant hemisphere and may include impaired ability to read, write and use gestures.
Wernicke’s dysphasia - lesions are located in temporal lobe specifically though to be in posterior section of superior temporal gyrus. Patients are unable to understand language speech is fluent but lacking content. Patients lack awareness of the speech difficulties and my get agitated
Broca’s dysphasia - lesions are located in the frontal lobe, also known as expressive dysphasia as patient are unable to speak fluently, difficult to understand but comprehension is good. patients are aware of their speech difficulties.
Conduction dysphasia - lesions around the arcuate fasciculus, posterior parietal and temporal regions. leads to naming deficits inability to repeat non meaningful words, although there is apparently normal speech comprehension and production.
Deep dysphasia - lesions are in the temporal lobe, symptoms are word repetition problems.
-Global dysphasia - occurs with extensive damage to basal ganglia, thalamus, symptoms are extensive with generalised deficits in comprehension, repetition, naming and speech production.
Name some of the visual fields defects and their causes
Bitemporal hemianopia - if upper quadrant affected more than lower = inferior chiasmal compression commonly due to pituitary tumour, if opposite way then superior chiasmal compression, commonly a cranipharyngioma.
Homonymous hemianopia with macular sparing = lesion of occipital cortex. Homonymous hemianopia with incongruous defects tends to be optic tract lesion where as congruous defects point towards optic radiation of occipital lesion.
Homonymous quadrantopias:
-superior = lesion of temporal lobe
-inferior = lesion of parietal lobe
Remember PITS Posterior-Inferior, Temporal-Superior
Describe the spinothalamic tracts and their journey through the CNS.
Spinothalamic tracts carries information related to pain, temperature, non-discriminative touch, and pressure.
Primary afferent fibres synapse in the contralateral dorsal horn, secondary neurones decussate through the ventral white commissure to the spinothalamic tract which lies ventral and lateral to the ventral horn.
From here the tract ascend, and in the brainstem fibres run in close proximity to the medial lemniscus and are known as the spinal lemniscus.
The majority of secondary fibres terminate in the ventral posterior nucleus of the thalamus, contacting third-order thalamocortical neurones that project to the somatosensory cortex.
Describe the dorsal columns and their journey through the CNS.
The dorsal columns are split into two tracts, the fasciculus gracilis (medial) and the fasciculus cuneatus (lateral). The tracts carry impulse concerned with proprioception and discriminative touch.
The dorsal columns contain axons of primary afferent neurones that have entered the cord through the dorsal roots. The fasciculus gracilis consits of fibres that join the cord at the sacral, lumbar and lower thoracic levels (lower limb) and the fasciculus cuneatus those from upper thoracic and cervical roots (upper limb). They travel on the ipsilateral side to the medulla oblongata where they terminate upon second-order neurones in the nucleus gracilis and cuneatus.
Second-order accons then decusste in the medulla as internal arcuate fibres and thereafter ascend through the brain stema s the medial lemniscus to terminate in the ventral posterior nucleus of the thalamus.
Third-order thalamocortical neurones in turn project to the somatosensory cortex located in the postcentral gyrus of the parietal lobe.
Describe the corticospinal tracts and their journey through the CNS.
A descending spinal tract concerned with the control of voluntary, discrete, skilled movements, especially those of the distal parts of the limbs
Primary neurones arise from motor and sensory parts of the cortex but the largest axons arise from betz cells in the premotor cortex in the precentral gyrus.
Corticospinal axons leave the cerebral hemisphers by passing through the corona radiate and internal capsule to entre the crus cerebri of the midbrain. Having passed through the the ventral portion of the pons, fibres reach the medulla oblongata where they form the pyrmiadal tracts on the ventral surface. In the caudal medulla majority of fibres decussate and travel down to cord in lateral corticospinal tracts however some remain ipsilateral as the ventral corticospinal tract which decussate lower down the cord.
Describe normal pressure hydrocephalus, its signs and symptoms, investigations, and treatment
Type of brain malfunction caused by decreased absorption of CSF typically presenting with the triad, ataxia, urinary incontinence and dementia. The dementia is predominantly frontal lobe in nature i.e. presents in the form of apathy, forgetfulness inertia, inattention.
Investigations:
- CT or MRI to exclude SOLs, shows enlarged ventricles
- lumbar puncture and evaluation of response to CSF removal.
Treatment:
-Surgical implantation of a ventriculoperitoneal shunt if clinically fit for surgery.
Describe stroke, its causes, risk factors, signs, and management
Strokes result from ischaemia infarction of bleeding into part of the brain, and manifest by rapid-onset of focal CNS signs and symptoms
Causes:
- Small vessel occlusion, cerebral microangiopathy of thrombosis insitu
- Cardiac emboli e.g. AF, endocarditis, MI
- Atherothromboembolism e.g. from carotids
- CNS bleeds e.g. hypertension, trauma, aneurysm rupture, anticoagulation, thrombolysis.
- sudden BP drop
- carotid artery dissection
- vasculitis
Risk factors: hypertension, DM, heart disease, PVD, past TIA, carotid bruit, the pill, hyperlipidaemia, alcohol abuse, pro-thrombotic disorders
Signs: sudden onset with progression over hours
- Cerebral infarcts: the following criteria should be assessed 3 of the below defines a TACI (middle and anterior cerebral arteries) and 2 of the below defines a PACI (smaller arteries of anterior circulation)
1) Unilateral hemiparesis and/or hemisensory loss of the face, arm and leg.
2) Homonymous hemianopia
3) high cognitive dysfunction e.g. Dysphasia. - Brainstem infarcts: quadriplegia, locked-in syndrome
- Lacunar infarcts: in basal ganglia, thalamus, and pons. ataxic hemiparesis, pure motor, pure sensory, sensorimotor and dysarthria/clumsy hand.
Management:
- Protect airway to avoid hypoxia/aspiration
- Pulse, BP, ECG - exclude AF, haemodynamically stable treat hypo not hypertension
- BM
- Urgent CT/MRI if thrombolysis considered, cerebellar stroke, unusual presentation,
- Consider thrombolysis if haemorrhagic stroke excluded and onset of symptoms less than 4.5hrs ago
- NBM keep hydrated assess speech and swallow
- Antiplatelet agents once haemorrhagic stroke excluded, aspirin 300mg for 2 weeks mono therapy then after 2 weeks dual antiplatlets.
- do not routinely anti-coagulate in ischaemic stroke due to risk of haemorrhagic transformation
- refer to stroke unit asap
- consider statin if hyperlipidaemia, controlling BP but not acutely unless thrombolysed in which case aim BP less than 180/110. In Haemorrhage aim BP less than 160/110. If no thrombolysis do not routinely treat BP unless over 220mmHg systolic. Seek Stroke nurse/specialist support.
Describe Guillain-Barre syndrome, its presentation, triggers, and management
Also known as acute inflammatory demyelinating polyneuropathy.
Presentation: Typically presents a few weeks after an infection with a symmetrical ascending muscle weakness. The trigger causes antibodies which attack nerves, though in 40% no cause is found. It may advance quickly, affecting all four limbs at once, and can lead to paralysis. There is a progressive phase of up to 4 weeks followed by recovery.
Management:
- lumbar puncture, CSF shows increased protein in absence of raised WCC.
- FVC monitoring 4 hourly with transfer to ITU if respiratory involvement.
- Cardiac monitoring required for risk of bradycardia or SVT
- Ventilate sooner rather than later e.g. if FVC less than 1.5L or signs of respiratory failure
- IV immunoglobulin 0.4g/kg/24h for 5d
Triggers include campylobacter jejuni, CMV, mycoplasma, zoster, HIV, EBV, vaccinations.
What is apraxia
A motor disorder cause by damage to the posterior parietal cortex leading to difficulty with motor planning to perform tasks or movements when asked.
Describe Vaso-vagal syncope, typical history,
Due to reflex bradycardia +/- peripheral vasodilatation provoked by emotion, pain, fear or standing too long. Onset is over seconds (not instantaneous), and is often preceded by nausea, pallor, sweating and closing in of visual fields (pre-syncope). It cannot occur when lying down. LOC for around 2 mins. Brief clonic jerking of the limbs may occur but there is no stiffening or tonic/clonic sequence. Urinary incontinence is uncommon but may occur, and there is no tongue-biting. Recovery is rapid.
Describe a circumducting gait and its causes
Patient stands with unilateral weakness on the affected side, arm held in flexion, adducted and internally rotated, leg extended on same side with plantar flexion of foot and toes. When walking the patient will hold his or her arm to onside and drag their affected leg in a semicircle (circumduction) due to weakness of distal muscles and extensor hypertonia.
This is most commonly seen in stroke.
describe a high-stepping gait and its causes
Seen in patients with foot drop (weakness of foot dorsiflexion), the cause of this gait is due to an attempt to lift the leg high enough during walking so that the foot does not drag on the floor.
If unilateral, causes include peroneal nerve palsy and L5 radiculopathy. If bilateral, causes include amyotrophic lateral sclerosis, Charcot-Marie-Tooth disease and other peripheral neuropathies including diabetic neuropathy.
Describe a myopathic (waddling) gait and its causes.
Hip girdles muscles are responsible for keeping the pelvis level when walking. If you have weakness on one side, this will lead to a drop in the pelvis on the contralateral side of the pelvis while-walking (Trendelenburg sign). with bilateral weakness, you will have drooping of the pelvis on both sides during walking leading to waddling
This gait is seen in patients with myopathies such as muscular dystrophy.
Describe the role of the hippocampus
Located in the medial temporal lobe of the brain, and part of the limbic system, the hippocampus plays important role in short-term memory, especially the conversion of short-term memory to long term, and spatial navigation
What is allodynia and name some causes?
Refers to triggering of pain response from stimuli which do not normally provoke pain.
Causes: Neuropathies, complex regional pain syndrome, fibromyalgia, migraine, spinal cord injury.
Describe Migraine, it’s symptoms, treatment, and prevention
A common cause of recurrent acute headaches.
Symptoms: Diagnostic criteria requires at least 3 attacks, of which last 4-72hours duration, and have at least 2 of the following characteristics; Unilateral, Moderate pain, pulsating quality, avoidance of physical activity. They must also have at least one of the following symptoms N+V, photophobia, phonophobia. And finally must not be attributable to another disorder. Classically headaches are preceded by an aura lasting 15-20minutes with onset of headache within an hour.
Aura:
Precedes headache by minutes and may persist during. May be visual such as chaotic lines or dots, visual distortion or scotomata, or hemianopia. May also be somatosensory such as paraesthesiae spreading from fingers to face. Motor aura such as dysarthria, ataxia, opthamolplegia or hemiparesis.
Treatment:
- NSAIDS (e.g. Ketoprofen 100mg PO, or dispersive aspirin 900mg/6h) are good as there is reduced chance of developing medication-misuse headache.
- Triptans such as rizatriptan may be used. They are CI if IHD, coronary spans, uncontrolled hypertension, recent lithium, SSRIs, or ergot use. SEs include arrhytmias and angina+/- MI
- Ergots may also be used such as ergotamine 1mg PO can cause gangrene and vascular damage. CI in those taking pill, PVD, IHD, pregnancy, breastfeeding, hemiplegic migraine, raynauds.
- Botulinum toxin type A injection may be used in chronic migraine headaches on more than 14days a month if no response to 3prophylactic drugs.
Prevention:
- Remove triggers I.e. CHOCOLATE, Hangovers, Orgasms, Cheese, Oral contraceptives, Lie-ins, Alcohol, Tumult, Exercise.
- If frequent I.e. More than 2 a month 1st line is propanolol 40-120mg/12h, amitriptyline 10-75mg nocte, or topiramate 25-50mg/12h
- 2nd line = valproate, pizotifen, gabapentin, pregabalin,
Describe Meralgia Paraesthetica, its symptoms, and management.
An entrapment syndrome of the lateral femoral nerve.
Symptoms: causes burning or numbness down the upper lateral aspect of the thigh. Pain can be reproduced by deep palpation just below the upper lateral aspect of the thigh.
Management:
- weight loss may cure the condition in the case of obesity
- otherwise NSAIDs may be trialled
What is cushings triad?
It is a sign of increased Intracranial pressure, it is a triad of Hypertension, bradycardia and irregular breathing
