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Motor Deficits and Weakness: History Taking and Differential Diagnoses

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Motor Deficits: Background

Overview

The descending tracts are mainly motor. The cell bodies of motor neurones are found in the cerebral cortex, brain stem, or spinal cord. Motor neurones convey impulses from these areas to muscles and glands. Motor neurones are divided into:

  • Upper motor neurones (UMNs):
    • Travel from the cerebral cortex through different tracts and synapse with lower motor neurones in the brainstem or spinal cord
    • UMNs can be further divided into:
      • The pyramidal tracts – voluntary control of body muscles (corticospinal tract) and face muscles (corticobulbar tract)
      • The extrapyramidal tracts – involuntary control of muscles involved in tone, balance, posture etc.
  • Lower motor neurones (LMNs):
    • Transmits signals from UMNs to the effector muscles to perform a movement

Upper motor neurones vs. lower motor neurones

UMNs travel from the cerebral cortex and synapse with LMNs in the brainstem or spinal cord. LMNs convey nerves to effector muscles. Therefore in general:

  • UMN lesions suggest a lesion in the central nervous system (CNS, brain and spinal cord)
  • LMN lesions suggest a lesion in the peripheral nervous system (PNS, anywhere that is not the brain and spinal cord)

Signs of upper motor neurone lesions

Signs and symptoms of UMN lesions can be divided into:

  • Negative symptoms:
    • Weakness
    • Decreased control
    • Easily fatigued
  • Positive symptoms:
    • Spasticity – velocity-dependent increased tone to passive stretch:
      • Quick movements of an affected limb result in increased tone
    • Clonus – rhythmic, involuntary muscle contractions when abrupt muscle stretch is applied
      • E.g. quick dorsiflexion of the foot leads to involuntary plantarflexion rhythmic movements
    • Hyperreflexia – brisk reflexes:
      • This is because UMNs are involved in providing inhibitory signals to LMNs
    • Pathological reflexes – such as:
      • The Babinski sign: stroking the sole of the foot leads to the extension of the large toe and fanning of the other toes – a positive Babinski sign
        • A normal response in adults is plantarflexion
      • The Hoffman sign: holding the patient’s middle finger and flicking the fingernail downward leads to flexion and adduction of the thumb – a positive Hoffman sign
        • This is seen in degenerative cervical myelopathy

Signs of upper motor neurone lesions

Although both UMN and LMN lesions result in weakness. LMN lesions have the following signs:

  • Decreased reflexes – reflexes may be absent
  • Decreased tone – muscles are weak or may be floppy
  • Muscle atrophy – muscles are wasting/thinning
  • Fasciculations – involuntary, rapid muscle twitches
  • Flaccid paralysis – paralysis and decreased tone

How do I know what side the motor lesion is on?

Most UMNs in the corticospinal tracts decussate (cross over) at the medulla and continue on the contralateral side to where they originated from before terminating in the brainstem or spinal cord where LMNs emerge.

Therefore, overall:

  • UMN lesions above the medulla cause contralateral signs
  • UMN lesions at/below the medulla cause ipsilateral signs
  • Since LMNs do not decussate, they cause ipsilateral signs.

Since nearly all cranial nerves are bilaterally innervated, unilateral UMN lesions do not usually cause problems except for CN VII (facial nerve) and CN XII (hypoglossal nerve). LMN lesions still cause ipsilateral signs.

  • CN VII:
    • Unilateral UMN lesions result in a lower facial droopaway from the side of the lesion
      • The upper half is unaffected as it is bilaterally innervated
    • LMN lesions would affect the ipsilateral side and involve both the upper and lower face
    • A patient presenting with a UMN lesion of the face, where only the lower face is affected, should raise suspicion of stroke
  • CN XII:
    • Unilateral UMN lesions result in tongue deviation away from the side of the lesion

History Taking

Overview

It might be difficult to take a history in a patient with acute motor deficits (e.g. if they have speech slurring or had a seizure), therefore, a collateral history may be necessary.

With each symptom, always (if relevant) ask about:

  • When did it start?
  • Did it come on suddenly or gradually?
    • Seconds, minutes, or hours – may suggest a vascular cause (e.g. stroke) or epilepsy
    • Subacutely over a few days – may suggest causes that are infective, compressive, or autoimmune/inflammatory
    • Episodic features may suggest an autoimmune/inflammatory cause
    • Over weeks-months may suggest a compressive problem
  • Is it continuous or intermittent?
  • Explore its timeline – is it getting better, worse, or staying the same?
  • Has this ever happened before?

Motor deficits

  • Have they had weakness or drooping?
  • Site – where is the weakness? (e.g. arms, legs, or face)
  • Ask about onset – was it sudden or gradual? Over how long?
  • Ask about duration
  • Ask about its timeline – is it getting, better, worse, or staying the same? 
  • Ask about its severity – (e.g. are they unable to stand up?
  • When were they last symptom-free?
  • What is the patient’s dominant hand?
    • This can give clues to the potentially affected site
    • If someone is right-handed, the lesion may be on the left side of the brain
  • Has there been any trauma?
  • Has there been any recent overseas travel? (may suggest infection such as encephalitis)

Neurological systems review

  • Screen for general features:
    • Any fever? – may suggest infection
    • Any constitutional symptoms? – may suggest malignancy
    • Any nausea and/or vomiting? – can suggest elevated intracranial pressure
  • Screen for associated stroke/transient ischaemic attack (TIA):
    • Facial drooping
    • Sensory problems (e.g. numbness or tingling)
    • Speech problems (e.g. slurring)
    • Visual problems
    • Ataxia, vertigo, or loss of balance
    • Confusion, drowsiness, or loss of consciousness
    • Headaches
    • Nausea and/or vomiting
    • Pain
  • Screen for headaches, seizures, and loss of consciousness:
    • Any headaches?
    • Any fits, falls, or funny turns?
    • Any confusion?
    • Any drowsiness?
    • Any problems with memory?
  • Screen for sensory problems:
    • Any visual changes?
    • Any changes in hearing?
    • Any numbness or tingling?
    • Any pain?
  • Screen for problems with balance and coordination:
    • Any problems with balance?
    • Any problems with coordination?
    • Any dizziness?
  • Screen for problems with speech, comprehension, and swallowing:
    • Any problems with speech? (e.g. slurring, problems ‘getting words out’ etc.)
    • Any problems understanding speech?
    • Any problems with memory?
    • Any problems with swallowing?
  • Other/autonomic:
    • Any loss of bowel/bladder control?

Past Medical History

Questions include:

  • Do they have any other medical conditions?
  • Have they ever had any previous surgery?
  • Do they take any regular medications?
  • Do they take any over-the-counter medications, herbal remedies, or supplements?

Family History

  • Is there any family history of anything similar?

Allergy History

  • Are they allergic to anything?
    • What happens during the allergic reaction?

Social History

  • Do they smoke?
    • If so, how much and how long?
  • Do they drink alcohol?
    • If so, how much and how long?
  • Do they use any illicit drugs?
    • If so, how much and how long?
  • What is their occupation?
  • Who’s at home?
    • What support do they have?
  • How has this impacted their activities of daily living?
  • Does the patient drive? – this is essential to ask:
    • The patient may need to stop driving and notify the DVLA

Physical Examinations

Overview

A complete neurological is essential. Some signs may include:

  • Vital signs:
    • Impaired level of consciousness and Glasgow Coma Scale
    • Fever, tachycardia, blood pressure abnormalities, reduced oxygen saturation
  • General inspection:
    • Muscle wasting and reduced muscle bulk
    • Fasciculations
    • Abnormal posturing
    • Involuntary movement (e.g. tremor, chorea etc.)
    • Pronator drift
  • Cranial nerves:
    • Eyes:
      • Visual field defects
      • Impaired eye movement
      • Impaired pupillary responses
      • Papilloedema
    • Facial nerve:
      • UMN – upper half of the face spared, should raise suspicion of stroke
      • LMN – all facial muscles are affected
    • Pharynx:
      • Deviation of the uvula away from the affected side
    • Tongue:
      • Fasciculation/wasting
      • Deviation – if UMN, it deviates away from the affected side
  • Speech:
  • Tone:
    • Features of a UMN lesion:
      • Increased tone
      • Spasticity
      • Ankle clonus (>5 beats)
    • Features of an LMN lesion:
      • Decreased tone
  • Power:
    • Reduced power
  • Reflexes:
    • Increased/brisk reflexes suggest a UMN lesion
    • Reduced/absent reflexes suggest an LMN lesion
    • Pathological reflexes (e.g. Babinski’s sign) may be present
  • Sensation:
    • May follow patterns (e.g. dermatomal or glove-and-stocking distribution)
    • Spinothalamic – reduced pain/temperature sensation
    • DCML – reduced vibration/proprioception
  • Vibration:
  • Coordination and gait:
    • May identify gait abnormalities
    • Coordination may be impaired (e.g. an inability to do the ‘heel-to-shin’ test or dysdiadochokinesia)
    • Romberg’s test may be positive

Investigations

Overview

Investigations are generally indicated if secondary headaches are likely. When suggesting investigations in an OSCE, the BOXES (Blood tests, Orifice tests, X-rays, ECGs, Special tests) mnemonic is useful for deciding the order of investigations:

  • Blood tests:
    • Blood glucose:
    • Full blood count (FBC):
      • To screen for anaemia, thrombocytopenia, or thrombocytosis
      • Leukocytosis may suggest inflammation/infection
    • Urea and electrolytes (U&Es):
    • C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR):
      • Non-specific markers of inflammation, may be elevated suggesting an infective or inflammatory cause
    • Lipid panel:
    • Coagulation panel:
    • Thrombophilia panel:
    • Creatine kinase (CK):
      • Often elevated in muscular dystrophies
    • Liver function tests:
    • Cardiac troponin:
      • To screen for concomitant myocardial ischaemia
  • ECGs and echocardiography:
    • ECG:
    • Echocardiogram:
      • If cardioembolic stroke is suspected
  • Special tests – generally CT is preferred first in acute scenarios due to speed:
    • Urgent non-contrast CT head:
      • To screen for haemorrhagic stroke. May show cerebral ischaemia, however, a normal CT head does not rule out a stroke
    • CT angiography:
      • If stroke is likely and the patient is eligible for thrombectomy
    • CT/MRI perfusion imaging:
      • To see if there is potential to salvage brain tissue, indicating the use of thrombectomy with/without thrombolysis in stroke
    • MRI:
      • Visualises soft tissue
    • Lumbar puncture:
      • If CNS infection or inflammation is suspected
    • Electroencephalogram (EEG):
      • May be used in seizures and encephalitis
    • Nerve conduction studies:
      • Can localise where a nerve injury is
    • Muscle biopsy:
      • Used for the diagnosis of dystrophies

Differential Diagnoses: Cerebrovascular & Metabolic

Stroke

  • History:
    • Symptoms occur over seconds, minutes, or hours
    • FAST features – Facial drooping, Arm/leg weakness, Speech (e.g. slurring, problems with comprehension) and swallowing problems
    • Sensory disturbances (numbness/tingling/pain), visual problems, loss of coordination and/or balance
  • Physical examination:
    • Arrhythmia, carotid bruit may be seen
    • Visual field defects, eye movement problems, cerebellar/speech dysfunction, weakness, abnormal sensation 
  • Investigations:
    • Blood glucose: no hypoglycaemia
    • ECG: may identify arrhythmia (e.g. atrial fibrillation)
    • Echocardiography: may identify cardioembolic source
    • Non-contrast CT head: may identify haemorrhage, infarction, or be normal
    • CT angiography: may identify occlusion
    • CT/MRI perfusion imaging: screens for salvageable brain tissue

Transient ischaemic attack

  • History:
    • Symptoms of stroke present but are often brief and often less than 1 hour 
  • Physical examination:
    • Transient stroke signs present
  • Investigations:
    • Blood glucose: no hypoglycaemia
    • ECG: may identify arrhythmia (e.g. atrial fibrillation)
    • Echocardiography: may identify cardioembolic source
    • Non-contrast CT head: normal
    • Diffusion-weighted MRI: no infarction

Hypoglycaemia

  • History:
    • History of diabetes, insulin administration, alcohol consumption
    • Sympathoadrenal symptoms (<3.3 mmol/L): sweating, anxiety, nausea, hunger, palpitations, tingling
    • Neuroglycopenic symptoms (<2.8 mmol/L): confusion, drowsiness, irritability, seizures, coma, focal neurological deficits
  • Investigations:
    • Blood glucose: <3.5 mmol/L

Extradural haematoma

  • History:
    • Head trauma followed by an immediate loss of consciousness and then regaining consciousness (the ‘lucid interval’) before losing it again as the haematoma expands
    • Associated headache, nausea, and vomiting
    • Coagulopathy or anticoagulant use may be present
  • Physical examination:
  • Investigations:
    • Non-contrast CT head: biconvex (lentiform) hyperdensity limited by skull suture lines

Subdural haematoma

  • History:
    • More common in neonates, the elderly, and chronic excess alcohol consumption
    • Acute – head trauma, headache, nausea, vomiting, fluctuating consciousness, seizures
    • Chronic – weeks-months of confusion, reduced consciousness, nausea, vomiting, focal neurological deficits, seizures
    • Coagulopathy or anticoagulant use may be present
  • Investigations:
    • Non-contrast CT head:
      • Acute: crescenteric hyperdensity that is not limited by skull suture lines
      • Chronic: crescenteric hypodensity that is not limited by skull suture lines

Subarachnoid haemorrhage

  • History:
    • Acute severe ‘thunderclap’ headache, often described as the worst headache ever felt, may be occipital, often reaches maximal intensity within 1-2 minutes, and may have sentinel headaches in the preceding 3 months
    • Hypertension, smoking, coagulopathy/anticoagulant use, autosomal dominant polycystic kidney disease, or family history may be present
  • Physical examination:
    • Meningismus – photophobia, neck stiffness
    • As the haemorrhage expands – altered consciousness, seizures, ‘surgical’ third nerve palsy (fixed, dilated pupil)
  • Investigations:
    • Non-contrast CT head: may show blood in the basal cisterns, fissures, and sulci
      • If within 6 hours and normal: consider alternate diagnosis
      • If >6 hours and normal: perform lumbar puncture within 12 hours – may show xanthochromia, confirming the diagnosis
    • Refer to neurosurgery if subarachnoid haemorrhage is diagnosed 

Differential Diagnoses: Traumatic & Compressive

Diffuse axonal injury

  • History:
    • Rapid acceleration and/or deceleration of the head (e.g. ‘shaken baby syndrome’, car accidents, falls etc.) causing traumatic shearing of axons
    • Often causes instant altered consciousness/coma
  • Physical examination:
    • Features are out of proportion to CT findings
    • Rapid deterioration of Glasgow coma score
    • Loss of pupillary reflexes, respiratory arrest, brain death
    • Patients often remain in a coma or a persistent vegetative state, some may have eye-opening after 2-3 weeks, and very few regain consciousness within the first year
  • Investigations:
    • CT head: often shows no significant findings, may show some oedema
    • MRI head: may identify micro-haemorrhages and oedema

Spinal cord compression

  • History:
    • May have a history of malignancy or trauma
    • Back pain is the earliest and most common symptom – may be worse when coughing/straining, progressive, constant and persistent when lying down, and may have nocturnal pain which may wake the patient from sleep
    • Neurological deficits include – lower limb weakness, numbness, tingling, urinary/bowel incontinence, saddle anaesthesia, erectile dysfunction
  • Physical examination:
    • Reduced sensation, tone, power, and anal sphincter tone
    • Reflexes tend to be increased below the level of the lesion and reduced/absent at the level of the lesion
  • Investigations:
    • Whole MRI spine: identifies the lesion

Spinal trauma

  • History:
    • History of trauma, osteoporosis, vertebral fractures, or malignancy may be present
    • Back pain that may persist when lying down or waking from sleep
    • Head/neck trauma should be considered a cervical spine injury unless proven otherwise – may have pain or restricted head movement, sensory deficits and weakness 
    • Focal vertebral tenderness at the level of injury
  • Investigations:
    • CT spine: identifies fracture, displacement, blood, or soft tissue lesions
    • MRI spine: assesses above in further detail

Compartment syndrome

  • History:
    • History of trauma, coagulopathy or anticoagulant use, intense sport, or limb compression
    • Pain – worse with both active and passive movement, may diminish over time due to reduced sensation due to impaired blood flow 
  • Physical examination:
    • Pain, paralysis, paraesthesia, pallor, or reduced/absent pulses may be seen
    • The limb may be swollen/tense and there may be evidence of injury (e.g. bruising)
  • Investigations:
    • Compartment pressure measurement: pressure >20 mmHg
    • Immediate fasciotomy: relieves pressure
    • Serum creatine kinase: may be elevated, suggesting muscle damage
    • X-rays: shows no signs of compartment syndrome, but can show associated bony pathology (e.g. fracture) 

Space-occupying lesion

  • History:
    • History of coagulopathy/anticoagulant use, brain infection/abscess, ionising radiation, neurofibromatosis, or tuberous sclerosis may be present
    • Headache that may start with waking, be nocturnal, worsen with coughing/straining/head movements
    • Associated nausea and/or vomiting
    • Changes in mental state – lethargy, irritability, confusion, drowsiness:
    • Frontal lobe lesions can cause personality changes/disinhibition, parietal lobe lesions can cause dysarthria
  • Physical examination:
    • ‘Surgical third nerve palsy’ – fixed, dilated pupil
    • Papilloedema, retinal haemorrhages
    • Gait abnormalities, sensory/motor/visual deficits, speech problems
  • Investigations:
    • CT head: may identify the underlying lesion
    • MRI head: can examine the lesion in more detail

Normal pressure hydrocephalus

  • History:
  • Investigations:
    • Non-contrast CT head: screens for space-occupying lesions, which may be normal or show ventricular enlargement
    • MRI head: shows ventricular enlargement

Differential Diagnoses: Infective

Meningitis

  • History:
    • Fever, headaches, neck stiffness, photophobia
    • Meningococcal septicaemia – non-blanching purpuric/petechial rash, hypotension, altered mental status
    • Elevated intracranial pressure can occur, resulting in nausea, vomiting, seizures, focal motor/sensory problems, altered consciousness, seizures
  • Physical examinations:
    • Kernig’s sign (~5%), Brudzinski’s sign (~5%)
    • If elevated intracranial pressure is present: focal motor/sensory deficits, papilloedema, seizures, altered consciousness 
  • Investigations:
    • Blood culture: identifies underlying organism
    • Lumbar puncture should be delayed if there is increased intracranial pressure due to the risk of herniation

Encephalitis

  • History:
    • Usually younger adults (around their 20s), may have a history of immunodeficiency, exposure to ill contacts, diabetes mellitus, systemic lupus erythematosus
    • Fever and psychiatric symptoms (altered consciousness, mood/personality changes, memory problems), seizures, nausea, and vomiting
  • Physical examination:
    • Fever, altered consciousness, seizures, lymphadenopathy, focal motor/sensory deficits, aphasia
  • Investigations:
    • FBC: may show leukocytosis
    • Blood culture: may identify bacterial causes (however ~90% of cases are viral)
    • Neuroimaging (CT/MRI brain): may be normal, may show changes in the medial temporal and inferior frontal regions (e.g. oedema, haemorrhage etc.)
    • Lumbar puncture and cerebrospinal fluid polymerase chain reaction (PCR): performed once elevated intracranial pressure is ruled out, findings depend on the underlying cause. In viral encephalitis, protein and lymphocytes are raised.
    • EEG: may show background slowing

Brain abscess

  • History:
    • History of upper respiratory tract infection (e.g. sinusitis), otitis media, neurosurgery, head trauma, meningitis, infective endocarditis (causing vegetation embolism), immunocompromise, or diabetes mellitus
    • Headache that is dull and persistent, fever, and features of elevated intracranial pressure (e.g. seizures, nausea/vomiting)
  • Physical examination:
    • Papilloedema, seizures, ‘surgical third nerve palsy’ (dilated, unreactive pupil), altered consciousness, sensory/motor deficits
  • Investigations:
    • FBC: may show leukocytosis
    • CRP/ESR: may be elevated
    • Blood culture: may be positive
    • CT/MRI head: may show rings of enhancement with surrounding oedema

Differential Diagnoses: Inflammatory & Autoimmune

Multiple sclerosis

  • History:
    • Usually women aged 20-40 years old, a history of optic neuritis may be present
    • Lethargy is one of the most common features
    • Visual problems – optic neuritis (most common presenting feature), Uhthoff’s phenomenon (worsening vision with rises in body temperature)
    • Sensory problems (paraesthesia, numbness, trigeminal neuralgia), motor problems (weakness, spasticity), balance problems, tremor
    • Urinary/bowel incontinence
  • Physical examination:
    • Lhermitte’s sign – shooting, electric-shock-like pain passing down the neck when flexing the neck
    • Sensory problems – paraesthesia, numbness 
    • Motor problems – weakness, spasticity, increased reflexes
    • Visual impairment, red desaturation, internuclear ophthalmoplegia
  • Investigations:
    • Contrast-enhanced MRI of the brain and spinal cord: identifies lesions
    • Lumbar puncture and cerebrospinal fluid analysis: may show oligoclonal bands

Guillain-Barré syndrome

  • History:
    • History of preceding viral/bacterial infection present (classically gastroenteritis), however, some people have no clear trigger
    • Develops over days and reaches its worst after around 1 week
    • Back/leg pain is often the first symptom
    • Progressive, symmetrical ascending muscle flaccid muscle weakness affecting the lower extremities first, starting proximally before moving inwards
    • Can progress to respiratory distress if chest muscles are involved
    • Sensory symptoms tend to be mild/absent, but some paraesthesia may be present
    • Miller-Fisher syndrome is a variant associated with eye muscle impairment first, followed by ataxia, weakness, and areflexia. Weakness may be descending instead of ascending.
  • Physical examination:
  • Investigations:
    • Lumbar puncture: albuminocytologic dissociation – raised protein with normal/slightly high white cell count
    • LFTs: aminotransferases may be slightly raised
    • Anti-GQ1b antibodies: present in Miller Fisher syndrome
    • Nerve conduction studies: show decreased motor nerve conduction speed

Myasthenia gravis

  • History:
    • Fatiguability – muscles progressively weaken during the day and with activity and improve with rest
    • Extraocular muscle weakness (drooping eyelids, double vision), dysphagia, dysarthria, proximal limb weakness
  • Physical examination:
    • Fatiguability can be replicated on examination by asking the patient to maintain an upward gaze
  • Investigations:
    • Serum acetylcholine receptor antibodies (anti-AChR): usually positive
    • Muscle-specific tyrosine kinase antibodies (anti-MuSK): may be positive
    • Single-fibre EMG: may identify reduced neuromuscular transmission
    • CT chest: to detect thymoma
    • Pulmonary function tests: measure FVC in acute myasthenic crisis, may be low

Lambert-Eaton myasthenic syndrome

  • History:
    • Primarily lower limb weakness, hyporeflexia, and autonomic dysfunction (orthostatic hypotension, impotence, urinary dysfunction, dry mouth/metallic taste)
    • Extraocular involvement is seen later than earlier (unlike myasthenia gravis)
    • Activity increases muscle strength
  • Physical examination:
    • Repetitive muscle contractions increase muscle strength
  • Investigations:
    • Anti-P/Q voltage-gated calcium channel antibodies: positive in LEMS
    • Acetylcholine receptor antibody (anti-AChR): negative in LEMS
    • EMG: repetitive nerve stimulation shows increasing responses
    • CT chest: may show underlying small-cell lung cancer

Vasculitis

Differential Diagnoses: Degenerative

Motor neurone disease

  • History:
    • Increasing muscle weakness with very few/no sensory signs, extraocular muscles are not usually affected, specific presentation varies depending on subtype (e.g. asymmetrical limb weakness in amyotrophic lateral sclerosis)
  • Physical examination:
    • A mixture of LMN and UMN signs, fasciculations, muscle atrophy
  • Investigations:
    • Diagnosis is clinical
    • Consider EMG: motor conduction is normal, slowing suggests an alternate diagnosis

Muscular dystrophies

  • History:
    • There may be a family history of muscular dystrophy, mostly seen in male people, delayed motor milestones, problems with walking, falling/clumsiness
    • There may be some degree of learning disability
  • Physical examination:
    • Calf hypertrophy, Gower’s sign may be positive, hypotonia
  • Investigations:
    • Serum creatine kinase (CK): elevated – due to muscle breakdown
    • Genetic testing: has now replaced muscle biopsy and identifies Xp21 mutations which correlate to the dystrophin gene

Differential Diagnoses: Other

Bell’s palsy

  • History:
    • Peak incidence is 15-40 years, drooping affecting the entire face
    • There may be post-auricular/facial pain, altered taste, dry eyes, and sensitivity to sound
  • Physical examination:
    • The entire face is affected (i.e. no forehead sparing), suggesting an LMN lesion
      • The forehead being spared suggests a UMN lesion and should raise suspicion of a stroke
  • Investigations:
    • Diagnosis is clinical

Ramsay-Hunt syndrome

  • History:
  • Physical examination:
    • The entire face is affected (i.e. no forehead sparing), suggesting an LMN lesion
      • The forehead being spared suggests a UMN lesion and should raise suspicion of a stroke
  • Investigations:
    • Diagnosis is clinical

Post-ictal paresis (Todd’s paresis)

  • History:
    • Transient weakness in a limb after a focal seizure affecting that limb
    • Usually resolves within 48 hours
    • There be associated post-ictal confusion, disorientation, and amnesia of the preceding seizure
  • Investigations:
    • Blood glucose: hypoglycaemia can cause provoked seizures
    • FBC: leukocytosis may suggest a central nervous system (CNS) infection
    • U&Es: hyponatraemia, hypernatraemia, and uraemia can cause seizures
    • ECG: to identify cardiac-related conditions that can mimic seizures
    • Toxicology screen: considered if illicit substances are suspected
      • Examples are cocaine, amfetamines, and opioids
    • EEG: may show epileptiform activity that corresponds with a specific epilepsy syndrome. A normal EEG does not rule out epilepsy.
    • Neuroimaging – ideally an MRI brain: to identify structural abnormalities, intracranial masses etc.

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