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Emergency Nursing Course. Neurological Emergencies Dr. Fu Tat Lee ( 李富達醫生 ) Princess Margaret Hospital ( 瑪嘉烈醫院 ). Outline. Neurological assessment Stroke Seizure Acute generalized weakness Headache. Neurological assessment. What is it? Where is it?. The Neurological Assessment.

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Emergency nursing course

Emergency Nursing Course

Neurological Emergencies

Dr. Fu Tat Lee


Princess Margaret Hospital




  • Neurological assessment

  • Stroke

  • Seizure

  • Acute generalized weakness

  • Headache

Neurological assessment

Neurological assessment

  • What is it?

  • Where is it?

The neurological assessment

The Neurological Assessment

  • History should direct the neurological examination to the most relevant areas.

  • Symptoms may occur before signs can be detected.

  • In the absence of symptoms, any signs are less likely to be important.

The neurological assessment1

The Neurological Assessment

  • Look for asymmetrical abnormalities

  • Tendon reflexes can be absent in health but may

    indicate an abnormality in the sensory or motor system

  • An EXTENSOR PLANTAR REFLEX which is reproducible is never normal (except in infants)

The neurological assessment2

The Neurological Assessment

A. Mental Status

Glasgow Coma Scaleeye opening

motor response

verbal response

B.Cranial nerves (1st - 12th)

C.Upper & lower limbs

- motor

- sensory

- coordination

- reflexes

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Decorticate posture

Decerebrate posture

Neurological examination

Neurological Examination

Cranial nerves

(1)1st (olfactory) nerve

- anosmia (loss of smell)

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2nd (optic) nerve

- visual acuity

- visual field

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Homonymous hemianopia

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Bitemporal hemianopia

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3rd (Oculomotor), 4th (Trochlear) and

6th (Abducent) nerves

- eye movements, upper eyelid & pupil size

5th trigeminal nerve

5th (Trigeminal) nerve

Motor: Masseter

Sensory: ophthalmic, maxillary & mandibular divisions

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VII nerve (Facial nerve)

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Lower Motor Neuron lesion of VII nerve palsy

Bell s palsy

Bell’s palsy

  • 1st described by Dr Charles Bell in 1882

  • Lower Motor neuron lesion of 7th nerve

  • idiopathic etiology

    -Dx on i) no identifiable cause (viral/post viral Sx)

    ii) peripheral



  • Pain

  • Tearing

  • Drooling

  • Hypersensitivity to sound

  • Impairment of taste

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  • DDx:Central 7th nerve palsy - sparing ipsilateral frontalis muscle

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Other causes of LMN lesion of VII nerve:

Acoustic neuroma

Parotid gland tumour

Ramsey Hunt Syndrome:

facial nerve palsy due to Herpes Zoster

vesicles at the external auditory canal and ear.

Bell s palsy1

Bell’s palsy

Treatment :- Prednisolone 60 mg daily for 5 days

- ? Acyclovir

- physiotherapy

- eyedrops and cover

- refer medical or ENT if fail to recover

Prognosis : 80% recover completely within 3 months

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8th (Acoustic) nerve

- balance

- deafness

Weber & Rinnie Test to distinguish conductive deafness

from sensory deafness

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Rinnie test

Weber test

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9th Glossopharyngeal nerve

Muscles for swallowing

10th vagus nerve

10th Vagus nerve

  • Smooth muscles of GI & respiratory tract

  • Pacemaker

  • Muscles of heart, pharynx & Larynx

gag reflex

(sensory 9th)

(motor 10th)

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11th (accessory) nerve

- sternomastoid & trapezius muscle

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12th (hypoglossal) nerve

- tongue

Neurological examination1

Neurological Examination

Upper & Lower limbs assessment


  • Posture, Muscle wasting, Fasciculation

  • Muscle Tone:Hypertonic or Hypotonic

  • Muscle power :

  • Grading :0complete paralysis

    Iflicker of contraction

    IImovement is possible where gravity


    IIImovement is possible against gravity

    but not if any further resistance is


    IVmovement is possible against gravity

    and some resistance

    Vnormal power

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  • Coordination

    Pastpointing, dysmetria, dysdiadochokinesia

    Romberg testing


  • Tendon Reflex

    Hyperreflexia or Hyporeflexia

  • Plantar Reflex

    Upgoing or Downgoing

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Line of Stroke

Normal Planter reflex

Barbinski reflex

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Signs of Upper Motor Neurone Lesions

  • Little muscles wasting unless from disuse

  • Spasticity + Clonus

  • Hyperreflexia

  • Extensor Plantar response

    Signs of Lower Motor Neurone Lesions

  • Wasting is prominent

  • Fasciculation

  • Hypotonia

  • Hyporeflexia

  • Normal or equivocal plantar reflex

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Light touch



Proprioception and vibration

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Assessment of brainstem function

Assessment of Brainstem function

Brainstem reflex

pupillary reactions

corneal responses

spontaneous eye movements

oculocephalic responses (Doll’s eye reflex)

oculo vesticular responses (Caloric test)

respiratory patterns

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  • Stroke is a syndrome of rapidly developing clinical symptoms and signs of focal or global disturbances of cerebral functions due to non-traumatic vascular causes, with symptoms lasting more than 24 hours.

  • Not a cerebrovascular “accident” but a consequence of cerebrovascular disease

Stroke is preventable

Stroke is preventable

  • Modifiable risk factors

    • History of stroke or TIA

    • Hypertension

    • Cardiac diseases

    • Atrial fibrillation

    • DM

    • Internal carotid artery stenosis

    • Smoking

    • Alcohol abuse

    • Hypercholesterolemia

    • Obesity

    • Lack of exercise

    • Haematological diseases, coagulopathies

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  • Major types of stroke

    • Ischaemic (70%)

      • Cortical

      • Subcortical

      • Posterior circulation

      • Lacunar infarction

    • Intracerebral haemorrhage (25%)

      • Supratentorial

      • Infratentorial

      • Both

    • Subarachnoid haemorrhage (5%)

Mortality morbidity

Mortality & Morbidity

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Circle of Willis

Principles of management

Principles of management

  • Assess vital signs

  • Confirm the diagnosis

  • Differentiate ischaemic from haemorrhagic stroke

  • Look out for clues for aetiology

  • Screen for early complications

Specific management of ischaemic stroke

Specific management of Ischaemic Stroke

Stroke is an emergency

Acute therapy is available for ischaemic stroke within 3 hours of onset.

Tissue Plasminogen activator (TPA) 0.9mg/kg

10% as bolus and 90% infusion over 1 hour

within 3 hours increases the proportion of patients with minimal or no disability by 13-16%

6% risk of transforming infarction into symptomatic haemorrhagic

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Antiplatelet therapy

Low dose Aspirin (160 to 300mg daily) within 48 hours

of onset prevents 11 recurrent ischaemic strokes or

deaths at the expense of 2 extra cases of haemorrhagic

transformation per thousand patients treated.

?? Glycoprotein IIb/IIIa inhibitor

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Spontaneous haemorrhagic transformation of infarction

commonly occurs within 2-4 days

Clinical trials not support indiscriminate use of


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  • Neurosurgery

    • Not needed in most cases

    • Obstructive hydrocephalus

    • Cerebellar haematoma or infarct

    • Large superficial or lobar haematoma

    • Markedly raised ICP

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-Primary epilepsy, idiopathic, onset before 20

-Secondary epilepsy, symptomatic, by parenchymal abnormality e.g. tumor, AVM, aneurysm, contusion/hematoma

Different types of seizure

Different types of seizure

-generalized/grand mal : witnessed LOC with generalized activities

-minor/petit mal (absence) : prolonged unresponsive staring without LOC, + focal muscular activity

-focal : repetitive motor activity without LOC

-temporal lobe : hallucinations (visual, auditory, and olfactory), memory loss, and/or bizarre behavior which may progress to focal-generalized motor activity

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-Todd’s paralysis - focal weakness/paralysis after seizure lasting up to several days

  • febrile convulsion :

    3 months to 5 years, rapidly rising fever

Clinical evaluation

Clinical evaluation


examine for trauma including head/facial

abrasions, contusions, lacerations, tongue,

buccal lacerations

Is patient seizing? Is patient awake?

Look for eye deviation and

focal/generalized tonic/clonic


Treat reversible causes

Treat reversible causes


H ypotension due to hypovolemia, arrhythmia

H ypoxia

H ypoglycemia

O verdose & others

(Electrolyte disturbance,Intracranial SOL,

CVA, Infection)

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mnemonics of “ A E I O U”“T I PS”

Status epileticus

Status epileticus

  • Traditional definition:

    • 30 minutes of continuous seizure activity or a series of seizures without return to full consciousness between the seizures.

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(D) Treatment

-support airway, IV, O2 and monitor

-treat reversible causes

1st line- Diazepam0.25mg/kg IV or

0.5mg/kg PR

- Lorazepam0.1mg/kg iv

- Midazolam0.1 mg - 0.3 mg/Kg IVI

or 0.2mg/kg IMI

2nd line - Phenytoin18 mg/Kg IV load at 50mg/min with cardiac monitoring

3rd line - Consider phenobarbitone (200mg=1ml=1 Ampule) imi, generalized anaesthesia



  • Breakthrough seizure

  • No underlying cause

  • No head or other serious injury

  • Good drug compliance

  • No recent change on medication

  • Escort by an responsible adult

Acute generalized weakness

Acute generalized weakness

  • Spinal cord compression

  • Neuropathies

    • Guillain-Barre syndrome

    • Metallic poisons (lead & arsenic)

    • Vitamin deficiencies (B12)

    • Systemic diseases (DM, Renal failure)

    • Drugs

Acute generalized weakness1

Acute generalized weakness

  • Motor end plate

    • Myasthenia gravis

    • Botulism

    • Eatom-Lambert syndrome

  • Myopathies

    • Acute periodic paralysis (Hyper, hypo or normokalemia)

    • Alcoholic myopathy

    • Polymyositis

    • Drug (steroid)

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Guillain Barre Syndrome(GBS)

George Charles Guillain

Jean Alexandre Barre

Guillain barre syndrome

Guillain Barre Syndrome

Pathology :An autoimmune disease causing

acute demyelinating inflammatory


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usually follow acute febrile illness, URTI, (days/weeks)

typical pattern : symmetrical ascending flaccid

motor paralysis, commonly with some sensory

Symptoms (tingling sensation)

Impaired breathing, BP and Heart rate


A&E patient with lower extremity weakness and loss of lower extremity reflexes

Investigations treatment

Investigations & treatment

  • Investigation

    • Nerve conduction test

    • CSF: high protein

  • Management (mainly supportive)

    • ICU care

    • Ventilatory & circulatory support

    • Plasmaparesis

    • High dose Ig

    • Psychological support

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  • 90% weakest at the 3rd week

  • Most patients recover

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What is the physical sign illustrated?

Myasthenia gravis

Myasthenia Gravis

-autoimmune disease

-antibodies against acetylcholine receptors at the neuromuscular junction of striated muscle


Myasthenia gravis1

Myasthenia Gravis

bimodal distribution in age and gender, 2nd/3rd decade female; 6th/7th decade male

-associated with thymic hyperplasia/thymoma

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  • complaints of muscle weakness, worsened byprolonged activity and improved with rest

  • most common begin with ocular ptosis, diplopia and blurred vision

  • Respiratory failure

  • Confirm by bedside Tensilon test (Endrophonium)

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  • Tension headache

  • Migraine

  • Cluster headache

  • Subarachnoid hemorrhage

  • Hypertension (DBP >130mmHg)

  • Meningitis

  • Space occupying lesion

  • Sinusitis

  • Acute Glaucoma

  • Postconcussion

  • Temporal arteritis

  • Trigeminal neuralgia

Possible causes

Possible causes

  • Intracranial

    • Hemorrhage

      • SAH, Subdural, Intracerebral

    • Tumour

    • Meningitis

    • Vessel

      • Migraine, Hypertension

  • Extracranial

    • Vessel

      • Temporal arteritis

    • Nerve

      • Trigeminal neuralgia

    • Muscle

      • Tension

    • Referred pain

      • Acute glaucoma, Sinusitis





  • Viral

  • Bacterial

    • Pneumococcus

    • Meningococcus

    • Haemophilus Influenzae Type B

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Kernig’s sign

Brudzinski’s sign

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Temporal arteritis

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Trigeminal Neuralgia

Watch out

Watch out !!!!

  • The first or the worst headache of patient’s life, especially the onset is acute and associated with neurology

  • Progressively gets worse over days or weeks and subacute in onset

  • Associated with fever, nausea and vomit

  • Associated with neck stiffness, focal neurology, papilloedema, and changes in conscious level and cognition

  • No obvious identifiable cause

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