Neurology Flashcards
What is a TACS, and what features must be present for diagnosis?
= a large cortical stroke affecting the areas of the brain suppled by both the middle & anterior cerebral artery territories.
- All three of the following must be present for a TACS diagnosis:
- Unilateral weakness (and/or sensory deficit) of the face, arm, and leg
- Homonymous hemianopia
- Higher cerebral dysfunction → dysphasia, visuospatial disorder.
What is a PACS & what must be present for a diagnosis?
= a less severe form of TACS, in which only part of the anterior circulation has been compromised.
- Two of the following need to be present for a PACS diagnosis:
- Unilateral weakness (and/or sensory deficit) of the face, arm, and leg
- Homonymous hemianopia
- Higher cerebral dysfunction → dysphasia, visuospatial disorder
What is a lacunar stroke (LACS) and what needs to be present for a diagnosis?
= a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions.
- One of the following needs to be present for LACS diagnosis:
- Pure sensory stroke
- Pure motor stroke
- Sensori-motor stroke
- Ataxic hemiparesis
How does a stroke involving the Anterior Cerebral Artery present? What is the key feature?
- Leg weakness is key !! Leg>arm/face weakness due to arrangement of the motor homunculus
- Sensory weakness → less common
- Motor aphasia → difficulty initiating speech, comprehension
- Urinary incontinence
How does a stroke involving the Middle Cerebral Artery present? What is the key feature?
-
Face/upper limb weakness
- Arm/Face > leg weakness
- Expressive aphasia → if lesion is on the dominant hemisphere, typically the left, due to Broca’s area being on the dominant side.
- Receptive aphasia → if lesion is on dominant hemisphere, due to Wernicke’s area being affected.
- Contralateral hemineglect → if the lesion is on the non-dominant side
What antiplatelet therapy is giving to people following an ischaemic stroke? What preparation can these be given?
Aspirin 300mg for 2 weeks (or until discharge).
- Change to 75mg clopidogrel OD after 2 weeks or once discharged.
- Oral, rectal, via NG tube
When can a patient be thrombolysed in the event of a stroke?
Alteplase can be used within 4.5hrs of symptom onset & once a haemorrhagic stroke has been ruled out on CT.
What secondary prevention is given following an ischaemic stroke long term?
- Clopidogrel 75mg OD
- Atorvastatin 20-80mg (after 48hrs)
- Blood pressure & diabetes control
- Address modifiable risk factors → smoking, obesity, exercise
When is an endarterectomy done following an ischaemic stroke?
If there is >50% occlusion on the affected side, and it can be done within a week
How does an extradural haematoma present?
- Often have immediate LOC, followed by period of lucidity, then a progressive decline in consciousness over the next few hours.
- Headache
- Nausea & vomiting
- Confusion
How does an extradural haematoma appear on a CT scan?
- Bi-Convex, lemon-shaped mass
- Midline shift
- Brainstem herniation
How does a subdural haematoma present?
- Drowsiness or poor balance & graduate deterioration following head trauma
- Headache
- Nausea & vomiting
How does a subdural haematoma show on CT scan?
- Crescent, banana-shaped mass
- Acute SDH → hyperdense (bright white) appearance
- Chronic SHD → hypodense (black/grey) appearance
How does a subarachnoid haemorrhage present?
- Sudden onset, severe headache (thunderclap)
- Nausea & vomiting
- Photophobia
- Kernig’s Sign → inability to extend the knee due to pain when the patient is supine & the hip & knee are flexed to 90 degrees
How does a subarachnoid haemorrhage show up on CT scan
- Hyperdensity around the Circle of Willis
- Hyperdensity in the subarachnoid space
What are the risk factors for idiopathic intracranial hypertension?
- Obesity
- Female
- Medications → COCP, tetracyclines, retinoids, lithium
What are the signs & symptoms of Idiopathic Intracranial Hypertension?
Symptoms → Chronic & progressive:
- Headache → non-specific, diffused, sometimes associated with nausea & vomiting. Typically worse in the morning or after bending forwards, or valsalva manoeuvres
- Transient visual loss / blurring of vision → lasts <30 seconds
- Pulsatile tinnitus → exacerbated by lying flat
- Visual disturbance → photophobia, flashes, transient visual darkening or loss
Signs:
- Bilateral papilloedema seen on fundoscopy
- Peripheral visual field defects
- Horizontal diplopia → due to a sixth nerve palsy in some cases
What is the key finding on lumbar puncture for Idiopathic Intracranial Hypertension?
elevated opening pressure >250mmH2O
How is Idiopathic Intracranial Hypertension managed?
Conservative Management:
- Weight loss
- Stop/change any medications which may be causing or worsening the IIH.
Medical Management:
- Considered in those with Mild-Moderate symptoms.
- Acetazolamide → carbonic anhydrase inhibitor which reduces the rate of CSF production
- If not tolerated, then topiramate or furosemide can be used.
- Serial lumbar punctures can be used short-term to preserve vision in patients with IIH awaiting a surgical procedure.
Surgical Management:
- Essential for IIH patients with rapidly declining visual function or those who failed medical therapy.
- CSF diversion procedures
What are the features of an essential tremor?
- Fine tremor (6-12Hz)
- Symmetrical
- Most notable in hands, but can affect the head, jaw, voice, tongue, face, lower limbs
- More prominent with voluntary movement
- Worse when tired, stressed or after caffeine
- Improved by alcohol
- Absent during sleep
How can an essential tremor be medically managed?
- Propranolol → first line, if patient is bothered by symptoms
- Primidone
What is clinically/radiologically isolated syndrome?
- Clinically IS = an otherwise unexplained clinical episode of neurologic dysfunction
- Radiologically IS = evidence of white matter pathology on neuroimaging not attributable to any other pathology in the absence of clinical symptoms.
What are the 3 main patterns of MS?
- Relapsing-Remitting MS
- Most common form of disease at presentation
- = unpredictable attacks of neurological dysfunction (>24hrs in absence of fever), followed by relief of symptoms, though patients may not return fully to baseline.
- Secondary Progressive MS
- Initially presents as relapsing-remitting, then later declines steadily & progressively without remission.
- Primary Progressive MS
- Steady, progressive worsening of disease severity from the onset without remission.
What is Lhermitte’s sign?
an electric shock sensation that travels down the spine & into the limbs when flexing the neck, indicating disease in the cervical spinal cord, caused by stretching the demyelinated dorsal column.
What are the two key investigations when diagnosing MS?
- MRI brain & spinal cord with gadolinium contrast
- MS lesions will be apparent as white matter plaques in T2.
- Need to be disseminated in space & space
- Oligoclonal bands in CSF & high protein content
- Reflect various immunoglobulins seen on CSF electrophoresis
How is an acute episode of MS managed?
- High-dose steroid therapy → methylprednisolone
- Plasmapheresis → if exacerbation is refractory to steroids
- Exclude any infections
What are the two first-line disease modifying therapies given in MS?
beta-inferon or glatiramer (injections)
What are the core features of Parkinson’s Disease?
-
Bradykinesia → key symptom
- Movements become slower & smaller
- Examples
- Handwriting gets smaller
- Shuffling gait
- Difficulty initiating movement
- Reduced facial movements & expressions (hypomimia)
-
Rigidity
- Resistance to passive movement of a joint
- Cogwheel rigidity in the arms
-
Tremor
- Worse on one side, 4-6 hertz, pill-rolling, worse when resting, improves with voluntary movement. Worse with distraction
-
Gait disturbance
- Shuffling, reduced arm swing, freezing
What are the types of generalised seizure?
- Tonic-Clonic (unconscious, muscle tensing then jerking)
- Myoclonic (conscious, sudden, brief muscle contractions)
- Atonic (conscious, sudden loss in muscle tone)
- Absence (brief vacant episodes, 10-20s
What medication is given for generalised tonic-clonic seizures?
Men/eligible women -> sodium valproate
Women -> lamotrigine, levetiracetam
What medication is given for focal seizures?
Lamotrigine or levetiracetam
What medication is used for absence seizures?
Ethosuximide
What medication is used for myoclonic seizures?
Men & Eligible women -> sodium valproate
Women -> levetiracetam
How is status epilepticus managed?
Management:
- A-E: secure the airway, give high-flow oxygen, check BMs, gain IV access
- 1st line → benzodiazepine, repeat after 5-10 minutes if the seizure continues
- 2nd line → IV levetiracetam, phenytoin, sodium valproate
- 3rd line → general anaesthesia
Benzodiazepine Options:
- Buccal midazolam (10mg)
- Rectal diazepam (10mg)
- IV lorazepam (4mg)
What is Bell’s Palsy, and how does it present?
= idiopathic syndrome that presents as a lower motor neuron facial palsy.
Presentation:
- Acute onset of unilateral LMN weakness → entire unilateral facial weakness
- Mild-moderate postauricular otalgia, which may precede the paralysis.
- Hyperacusis → disorder in loudness perception, overly sensitive to a range of sounds.
How is Bell’s Palsy managed?
- If patient presents within 72hrs of developing symptoms:
- Prednisolone → 50mg for 10 days, or 60mg 5 days followed by a reducing regime.
- Lubricating eye drops & tape eye closed at night.
What is trigeminal neuralgia?
= chronic neuropathic pain, characterised by a sharp shooting sensation affecting the face in the distribution of the trigeminal nerve (CNV).
How does trigeminal neuralgia present?
- Unilateral, sharp facial pain → burning, shooting, stabbing
- Triggers → talking, washing the face, shaving, brushing teeth, exposure to cold air
- Ophthalmic symptoms occasionally → lacrimation, conjunctival redness, photophobia
How is trigeminal neuralgia managed?
Medical:
- Carbamazepine is first line
- Other choices are phenytoin, lamotrigine, gabapentin
Surgical:
- Decompression or ablation of nerve.
- Microvascular decompression
- Treat any underlying causes such as tumours.
What are the features of Chronic Fatigue Syndrome?
- Extreme fatigue, which is not significantly relieved by rest
- Post-exertional malaise
- Sleep disturbances → broken or shallow sleep, altered sleep pattern, feeling exhausted, flu-like & stiff on waking.
- Cognitive impairment
How do tension-headaches present?
- Bilateral, non-pulsatile dull pain
- Constant pressure, like having a tight band around the head.
- Scalp muscle tenderness -> around the scalp, neck, or shoulder muscles on palpation
- Triggers: stress, depression, alcohol, skipping meals, dehydration.
How are tension headaches managed?
- Reassurance
- Simple analgesia
- Stress management
- Physio: massage or muscle relaxation exercises.
- Amitriptyline for chronic or frequent tension headaches.
What is cervical spondylosis? How does it present?
= age-related degeneration of the cervical spine, leading to pain & disability.
- Neck pain, made worse by movement
- Headaches
- Radiculopathy: due to compression of nerve roots, leading to flaccid upper limb paralysis.
What are cluster headaches? How do they present?
= a primary headache disorder that presents with severe unilateral headaches associated with a number of autonomic symptoms.
- Severe, unilateral, intra or supra-orbitally. Patients need to rock or sway to distract themselves from the pain.
- Red, swollen, watering eye
- Miosis (pupil constriction)
- Ptosis
- Nasal discharge
- Facial sweating
How are cluster headaches managed?
Prophylaxis -> verapamil 1st line, topirimate, lithium
Acute attack -> triptans (subcut or nasal), high-flow 100% oxygen
How is an acute migraine managed?
- NSAIDs
- Paracetamol
- Triptans -> avoid in patients with ischaemic heart disease, as triptans cause vasoconstriction.
- Antiemetics
NB: opiates may make the condition worse.
What prophylactic management is given for migraines?
- avoid triggers
- Propranolol - 1st line
- amitriptyline
- topiramate
What is myasthenia gravis?
= an autoimmune condition affecting the neuromuscular junction (NMJ), causing muscle weakness that progressively worsens with activity & improves with rest.
What is the pathophysiology of myasthenia gravis?
- Acetylcholine receptor (AChR) antibodies are found in most patients with MG.
- These antibodies bind to the postsynaptic ACh receptors, blocking them & preventing stimulation by ACh.
- The more the receptors are used during muscle activity, the more blocked they become.
- There is less effective stimulation of the muscle with increased muscle activity.
- With rest, the receptors are cleared & the symptoms improve.
- These antibodies also activate the complement system within the NMJ, leading to cell damage at the postsynaptic membrane, further worsening symptoms
How does myasthenia gravis present?
Muscle weakness that worsens with use, improves with rest
- Commonly proximal muscles of limbs & small muscles of head/neck.
- Difficulty climbing stairs, standing from seat, raising hands above head
- Diplopia → extraocular muscle weakness
- Ptosis → eyelid weakness
- Weakness in facial movements
- Difficulty swallowing
- Fatigue in jaw when chewing
- Slurred speech
What test can be performed when there is diagnostic uncertainty with myasthenia gravis? How is it performed?
Edrophonium Test:
- Give IV edrophonium chloride (or neostigmine).
- Normally cholinesterase enzymes in NMJ break down acetylcholine → edrophonium blocks these enzymes, reducing the breakdown of ACh.
- Therefore ACh level rises at the NMJ, temporarily relieving the weakness.
- A positive result suggests a diagnosis of MG.
How is myasthenia gravis managed?
- Pyridostigmine → cholinesterase inhibitor, prolongs action of ACh & improves symptoms
- Immunosuppression → eg, prednisolone, azathioprine, suppresses the production of antibodies
- Thymectomy → can improve symptoms, even in patients without a thymoma
- Rituximab → monoclonal antibody against B cells
What is a myasthenic crisis & how is it managed?
= A potentially life-threatening complication of MG
- Causes an acute worsening of symptoms, often triggered by another illness, such as an URTI.
- Respiratory muscle weakness can lead to respiratory failure → patients may require non-invasive ventilation or mechanical ventilation.
- Treat with IV immunoglobulins & plasmapheresis
What are the components of GCS?
Eye (4)
4 - spontaneous
3 - sound
2 - pressure
1 - no response
Verbal (5)
5 - orientated
4 - confused
3 - words
2 - sounds
1 - no response
Motor (6)
6 - obey commands
5 - localising to pressure
4 - normal flexion (withdraws to pain)
3 - abnormal flexion
2 - abnormal extension
1 - no response
What is the most common cause of encephalitis?
HSV-1
How is encephalitis managed?
- 2g IV ceftriaxone BD
- High dose IV acyclovir:
- 10mg/kg TDS
- Continue for 14 days then repeat LP
- If HSV PCR negative, stop further treatment. If positive, then give a further 7 days and repeat LP.
How does a brain abscess present?
Classic Triad:
- Headache
- Fever
- Focal neurological signs
Other Presentations:
- Nausea & vomiting
- Meningism
- Papilloedema
How is a brain abscess managed?
- Neurosurgical intervention for drainage
- Empirical antibiotics → IV ceftriaxone & IV metronidazole
At what vertebral level does spinal cord compression become referred to as cauda equina syndrome?
L3 onwards, as the spinal cord ends around L2
How does spinal cord compression present?
- Back pain → delayed diagnosis
- Localised, gradually increasing, worse on straining, waking up from sleep.
- Weakness (UMN pattern)
- Hyper-reflexia, increased tone, muscle weakness.
- Different to cauda equina syndrome which shows a LMN pattern
- Sensory loss
- Bladder & bowel dysfunction
- Urinary retention
How is spinal cord compression managed?
- Immediate practical measures → lie flat, neutral spine alignment, analgesia, high dose steroids.
- Palliative mostly → indicative of advanced metastatic cancer
- Definitive → radiotherapy (symptom control), surgery (laminectomy), chemotherapy
How does cauda equina syndrome present?
Symptoms:
- Severe back pain
- Bilateral sciatica
- Perianal anaesthesia
- Bowel & bladder dysfunction (urinary retention)
- Sexual dysfunction
Symptoms (LMN signs):
- Hypotonia
- bilateral or unilateral weakness
- areflexia
- abnormal sensory changes
- reduced anal sphincter tone/loss of anal squeeze
How does an UMN lesion present?
An UMN lesion will be in the CNS (brain & spinal cord).
- The CNS is involved in suppressing pathway activity → helps in the conscious inhibition of muscle
- If we damage UMNs, there is a loss of inhibitory tone of muscles, leading to constant contraction.
On examination:
- Minimal atrophy
- Increased tone (spasticity/rigidity)
- Ankle clonus
- Pyramidal pattern of weakness → extensors weaker than flexors in arms, vice versa in legs
- Hyper-reflexia
- Upgoing plantars → babkinski sign
How does a LMN lesion present?
An LMN lesion affects anywhere from the anterior horn cell to the muscle.
- If LMNs are damaged/lost, there is nothing to tell the muscles to contract.
On examination:
- Marked atrophy
- Fasciculations
- Reduced tone
- Variable patterns of weakness
- Reduced or absent reflexes
- Downgoing plantars or absent response.
What are the two most common times of MND?
- Amyotrophic lateral sclerosis (ALS) → most common & well-known type of MND
- Progressive bulbar palsy → second most common form, and primarily affects the muscles of talking & swallowing.
How does MND present?
Typically manifests as a combination of upper & lower motor neuron signs.
- If there are any sensory changes, an alternative diagnosis should be considered.
Symptoms:
- Insidious, progressive weakness of the muscles throughout the body
- Limbs, trunk, face, speech
- Increased fatigue when exercising
- Clumsiness, dropping things more often, tripping over
- Slurred speech → dysarthria
Signs:
- LMN disease
- Muscle wasting
- Reduced tone
- Fasciculations
- Reduced reflexes
- UMN disease
- Increased tone or spasticity
- Brisk reflexes
- Upgoing plantar reflex
How is MND managed?
There are no effective treatments for halting or reversing the progression of MND.
Supportive:
- MDT input
- Symptom control → pain relief, baclofen for muscle spasticity, antimuscarinic for excessive saliva
- Benzodiazepines → for breathlessness worsened by anxiety
- Palliative care
Medical:
- Non-invasive ventilation → to support breathing when the respiratory muscles weaken
- Riluzole → can slow the progression of disease & extend life by an average of 3 months.
