Unilateral Weakness Flashcards
TIA presentation
The person presents with sudden onset, focal neurological deficit which has completely resolved within 24 hours of onset and cannot be explained by another condition such as hypoglycaemia.
Most TIAs are thought to resolve within 1 hour but can persist for up to 24 hours.
Focal neurological deficits may include:
Unilateral weakness or sensory loss.
Dysphasia.
Ataxia, vertigo, or loss of balance.
Syncope.
Sudden transient loss of vision in one eye (amaurosis fugax), diplopia, or homonymous hemianopia.
Cranial nerve defects.
Initial management of suspected and confirmed TIA
Giving aspirin 300 mg immediately (unless contraindicated or taking aspirin regularly) and arranging specialist assessment within 24 hours if a suspected TIA has occurred within the last week.
Referral for specialist assessment as soon as possible within 7 days if the suspected TIA occurred more than 1 week previously.
Advising the person not to drive until definitive guidance is given by a specialist.
After a TIA, follow up should be arranged to optimize secondary prevention lifestyle and drug strategies.
Hospital:
Imaging - Do not offer CT brain scanning to people with a suspected TIA unless there is clinical suspicion of an alternative diagnosis that CT could detect.
After specialist assessment in the TIA clinic, consider MRI.
Carotid imaging - Everyone with TIA who after specialist assessment is considered as a candidate for carotid endarterectomy should have urgent carotid imaging + lifestyle advice.
Ensure that people with stable neurological symptoms from acute non-disabling stroke or TIA who have symptomatic carotid stenosis of less than 50% according to the NASCET criteria, or less than 70% according to the ECST criteria:
do not have surgery
receive best medical treatment (control of blood pressure, antiplatelet agents, cholesterol lowering through diet and drugs, lifestyle advice).
Thrombolectomy
Aspirin and anticoagulant therapy
Nutrition and hydration
Surgery
Bell’s palsy presentation
Acute, unilateral facial nerve weakness (upper and lower parts) or paralysis of rapid onset (less than 72 hours) and unknown cause.
This causes a reduction in movement on the affected side, often with drooping of the eyebrow and corner of the mouth and loss of the nasolabial fold.
Difficulty chewing, dry mouth, and changes in taste.
Incomplete eye closure, dry eye, eye pain, or excessive tearing.
Numbness or tingling of the cheek and/or mouth.
Speech articulation problems, drooling.
Hyperacusis.
Herpes simplex virus, varicella zoster virus, and autoimmunity may contribute.
A diagnosis of Bell’s palsy can be made when no other medical condition is found to be causing facial weakness or paralysis.
Features atypical of Bell’s palsy require referral for exclusion of an alternative diagnosis.
manage Bell’s palsy
The person should be advised to keep the affected eye lubricated by using eye drops during the day and ointment at night.
The eye should be taped closed at bedtime using microporous tape, if the ability to close the eye at night is impaired.
For people presenting within 72 hours of the onset of symptoms, prescription of prednisolone should be considered.
Antiviral treatment alone is not recommended, but it may have a small benefit in combination with a corticosteroid; specialist advice is recommended if this is being considered.
Urgent referral should be arranged if nerve palsy may be caused by:
An upper motor neurone cause.
Cancer.
Acute systemic or severe local infection.
Trauma.
Specialist Bell’s palsy
Referral to an appropriate specialist should be arranged if:
Ocular symptoms (for example, pain, irritation, or itch) develop at any time.
Atypical features are present.
There is no improvement after 3 weeks of treatment.
Existing neurologic findings worsen, or if new neurologic findings develop.
There is incomplete recovery after 3 months of onset of symptoms.
Referral should be considered for people who:
Have developed symptoms of aberrant reinnervation 5 months or more after the onset of Bell’s palsy.
May benefit from further support or counselling if there are emotional consequences of persistent facial paralysis or paresis.
Routine referral should not be arranged for adults with an uncomplicated episode of Bell’s palsy.
Management of a suspected acute stroke (or emergent TIA) in primary care
Immediate emergency admission to a stroke unit.
Provision of adequate advance information to ambulance control and the admitting hospital.
Avoidance of antiplatelet treatment until haemorrhagic stroke has been excluded.
After a stroke follow up should be arranged on discharge from hospital, at 6 months, and then annually to:
Assess the need for specialist review.
Assess the social and health care needs of the person and their family/carer.
Optimize lifestyle measures, and drug treatments for secondary prevention.
Stroke presentation
The person presents with sudden onset, focal neurological deficit which is ongoing or has persisted for longer than 24 hours and cannot be explained by another condition such as hypoglycaemia.
The clinical features of stroke vary depending on causative mechanism and the area of the brain affected:
Confusion, altered level of consciousness, and coma.
Headache — usually of insidious onset and gradually increasing intensity in intracranial haemorrhage, and sudden, severe headache in subarachnoid haemorrhage which may be associated with neck stiffness.
Sentinel headache(s) may occur in the preceding weeks.
Unilateral weakness or paralysis in the face, arm, or leg.
Sensory loss — paraesthesia or numbness.
Ataxia.
Dysphasia.
Dysarthria.
Visual disturbance — homonymous hemianopia, diplopia.
Gaze paresis — this is often horizontal and unidirectional.
Photophobia.
Dizziness, vertigo, or loss of balance — isolated dizziness is not usually a symptom of TIA.
Nausea and/or vomiting.
Specific cranial nerve deficits such as unilateral tongue weakness or Horner’s syndrome (miosis, ptosis, and facial anhidrosis).
Difficulty with fine motor coordination and gait.
Neck or facial pain (associated with arterial dissection).
Posterior circulation strokes may be difficult to diagnose and should be suspected if the person presents with:
Symptoms of acute vestibular syndrome — acute, persistent, continuous vertigo or dizziness with nystagmus, nausea or vomiting, head motion intolerance, and new gait unsteadiness.
Stroke assessment
Examine the person to assess:
The level of consciousness using the Glasgow Coma Scale.
Airway, breathing, and circulation (ABC).
Vital signs including blood pressure, heart rate, oxygen saturation, and temperature.
Carry out a focused neurological examination.
Look for clinical signs of stroke or TIA such as unilateral weakness, visual or speech disturbance, ataxia, and nystagmus.
Use the Face Arm Speech Test (FAST) validated tool for rapid assessment.
Suspect stroke if one or more of the following are present: new facial weakness (asymmetry such as the mouth or eye drooping), arm or leg weakness, or speech disturbance (such as slurring or difficulty in finding names for commonplace objects).
CVS exam — auscultate the heart to check for arrhythmia, murmurs, or pulmonary oedema and look for signs of CVD, such as heart failure.
General health — look for signs of trauma, coagulopathy, and other risk factors.
Carry out appropriate investigations where this does not cause delay in transport to hospital:
Check blood glucose with a glucometer to rule out hypoglycaemia (blood glucose less than 3.3 mmol/L).
Electrocardiogram (ECG) to exclude arrhythmias.
Stroke and tia history
Take a focused history from the person and, if possible, a collateral history from witnesses or family members.
Ask about:
Clinical features including focal neurological deficits and associated symptoms such as headache, vomiting, or decreased level of consciousness.
Time of onset, speed of onset (sudden or gradual), duration, intensity, and fluctuation of symptoms.
Time from stroke onset is essential to determine eligibility for acute stroke treatments such as tissue plasminogen activator (tPA).
If time of onset is not clear ask what time the person was last known to be unaffected (at their previous baseline or symptom-free state). If the person awoke with symptoms the time of onset is defined as when the patient was last awake and symptom-free.
In general, symptoms will have completely resolved in people with TIA and persist in people with stroke.
Other features that may indicate an alternative diagnosis such as migraine, giant cell arteritis, or seizures.
Risk factors for stroke and TIA.
Comorbid medical conditions, including liver disease, cancer, haematological disorders, or dementia.
Past medical history of stroke or TIA, miscarriage, or thromboembolic events suggesting inherited or acquired thrombophilia.
Recent trauma or surgery.
Family history of stroke — this may indicate familial hyperlipidaemia or hypercoagulability.
Current medications such as anticoagulants, insulin, or antihypertensive.
Stroke and tia history
Take a focused history from the person and, if possible, a collateral history from witnesses or family members.
Ask about:
Clinical features including focal neurological deficits and associated symptoms such as headache, vomiting, or decreased level of consciousness.
Time of onset, speed of onset (sudden or gradual), duration, intensity, and fluctuation of symptoms.
Time from stroke onset is essential to determine eligibility for acute stroke treatments such as tissue plasminogen activator (tPA).
If time of onset is not clear ask what time the person was last known to be unaffected (at their previous baseline or symptom-free state). If the person awoke with symptoms the time of onset is defined as when the patient was last awake and symptom-free.
In general, symptoms will have completely resolved in people with TIA and persist in people with stroke.
Other features that may indicate an alternative diagnosis such as migraine, giant cell arteritis, or seizures.
Risk factors for stroke and TIA.
Comorbid medical conditions, including liver disease, cancer, haematological disorders, or dementia.
Past medical history of stroke or TIA, miscarriage, or thromboembolic events suggesting inherited or acquired thrombophilia.
Recent trauma or surgery.
Family history of stroke — this may indicate familial hyperlipidaemia or hypercoagulability.
Current medications such as anticoagulants, insulin, or antihypertensive.
DDx
Many conditions (sometimes known as stroke mimics) can present with similar clinical features to stroke and TIA.
Toxic/metabolic disturbance such as:
Hypoglycaemia.
Drug and alcohol toxicity.
Conditions which can cause dizziness or disturbed balance such as:
Syncope.
Labyrinthine disorders — vertigo, Meniere’s disease, labyrinthitis.
Neurological conditions such as:
Seizure.
Migraine with aura.
Demyelination — multiple sclerosis.
Peripheral neuropathies such as Bell’s palsy.
Spinal epidural haematoma.
Trauma
Systemic or local infection including:
Central nervous system abscess.
Encephalitis.
Sepsis.
Encephalopathies such as:
Hypertensive encephalopathy.
Wernicke’s encephalopathy.
Space occupying lesions including:
Tumour.
Subdural haematoma.
Other conditions such as:
Acute confusional state.
Dementia.
Vasculitis.
Somatoform or conversion disorder.
