Neurological Conditions

Front 1

SEIZURES
Definition:

Back 1

A seizure is defined as a sudden, brief alteration of consciousness caused by abnormal neuronal activity in the brain. Seizure activity may causes motor, sensory, cognitive, psychic, or autonomic disturbances. Pt presentation may range from obvious convulsions to abnormal behaviours.

Front 2

SEIZURES
Aetiology:

Back 2

Epilepsy:
describes a number of syndromes which present with recurrent seizures, with diagnosis requiring a history of 2 or more unprovoked seizures. Triggers in epilepsy can include:

-Lack of sleep / stress
-Sudden stopping or changing medication
-Fever / infection / viruses
-Diarrheoa and vomiting, dehydration
-Allergies
-Alcohol / Illicit drug use
-Menstruation
-Photosensitivity
-Extreme temperatures, particularly heat
-Electrolyte disturbances

Provoked seizures result from a recognisable cause. Such as:
-Hypoxia
-Hypotension
-Metabolic (hypoglycaemia, hyponatremia, hypocalcaemia, hyperthyroidism, uraemia)
-Pregnancy – eclampsia
-Meningitis / encephalitis
-Hyperthermia / febrile convulsions
-Drugs / toxins (withdrawal including alcohol, overdose, poisons)
-Cerebral pathology (tumour, stroke, trauma).

Pseudoseizures are where seizure activity is psychological in origin, not from a neuronal disruption. This patient may be unaware of the cause of the seizure.

Front 3

SEIZURES
Pathophysiology:

Back 3

Partial seizures:
are where excessive neural activity occurs or begins in one region of the cerebral cortex. These can be classified as:
-Simple partial – seizure activity that does not impair consciousness
-Complex partial – occurs in one part of the brain however it is characterised by impaired consciousness. There types of seizures may be preceded by simple partial seizures.

Generalised seizures are where the neural activity involves the whole cortex, conscious level is affected. These can be:
-Absense – characterised by a usually brief lapse in consciousness and pause in activity.
-Atonic – is one of two generalised seizures referred to as “drop attacks”. Atonic seizures are characterised by sudden loss of consciousness and muscle tone.
-Tonic – also referred to as a “drop attack” characterised by loss of consciousness and increased muscle tone.
-Clonic – characterised by loss of consciousness with bilateral jerking without stiffening.
-Myoclonic – a brief sudden jerking action usually of one muscle or one muscle group in the upper body.
-Tonic clonic – the loss of consciousness is concurrent with tonic (stiffening) followed by clonic (jerking) actions.

Status Epilepticus:
is a medical emergency. It is defined as seizure activity >5mins or a continuous state of seizures where one seizure follows another and the patient does not recover to a GCS of 15 before the next seizure occurs. Status can occur in almost any seizure type.

Front 4

SEIZURES
Signs/Symptoms:

Back 4

Typical presentations in seizures:
-Visual hallucinations with formed images or flashes of light, déjà vu, unusual sensory disturbance
-Localised twitching and numbness
-Nonsensical speech
-Disorientated movements
-Sudden pause in activity or fixed gaze
-Nystagmus
-Automatism
-Increase or loss of tone including trismus
-Alternating tonic / clonic posturing
-ALOC
-Incontinence
-Post – ictal: confusion, fatigue, headache, nausea

Seizure activity in children manifest differently in children including:
-Vacant stare
-Lack of gross muscle tonicity
-Nystagmus, lateral fixed gaze and / or facial muscle twitching

Prolonged seizures or status epilepticus are associated with:
-hypoxia, hypercarbia
-Progressive lactic and respiratory acidosis
-Hyperthermia, hypertension, tachycardia
-Hypo / hyperglycemia
-Hyperkalaemia

Front 5

SEIZURES
Treatment:

Back 5

-Standard cares
-Reassurance
-Oxygen
Posturing
-Airway
-Midazolam
-IPPV
-Treat reversible cause (eg hypoglycaemia, hyperthermia, respiratory acidosis)

Front 6

Autonomic Dysreflexia
Definition:

Back 6

Autonomic dysreflexia is serious condition in patients with an existing, non-acute, spinal cord injury above the level of T6. It is characterised by a sympathetic response that goes unchallenged leading to a hypertensive crisis.

Front 7

Autonomic Dysreflexia
Aetiology:

Back 7

This condition can be caused by a number of noxious stimuli including:
-Distended bladder due to blocked / kinked catheter
-Urinary Tract Infection
-Bowel irritation (constipation / faecal impaction)
-Skin irritations (pressure sores, ingrown toe nails, burns, sunburn)
-Contracting uterus, fractures or any other event that would normally be deemed painful.

Front 8

Autonomic Dysreflexia
Pathophysiology:

Back 8

Is a condition that can occur in patients with non-acute spinal cord injury (SCI) at or above T6 level as a result of widespread reflex sympathetic over-activity including hypertension and vasoconstriction) below the level of injury in response to noxious stimuli which cannot be felt by the patient. The compensatory mechanisms (vasodilatation and bradycardia) are mediated by the vagus nerve. However the compensation is not sufficient to control the rising BP whilst the noxious (irritants, things which would ordinarily cause pain) stimulation remains. This results in a secondary hypertensive crisis.

Front 9

Autonomic Dysreflexia
Signs/symptoms:

Back 9

Clinical features:
-Flushing of skin above the level of injury – paleness below level of injury
-Relative hypertension (BP for quadriplegics and high level paraplegics is typically low when lying
and even lower when sitting (90-100 / 60 mmHg)
-Bradycardia
-Profuse sweating and goose bumps above the level of injury
-Pounding headache (worsening as BP rises)
-Blurred vision and headache
-Cardiac events including ACS, APO and stroke.

Front 10

Autonomic Dysreflexia
Treatment:

Back 10

-Standard cares
-Position upright with legs dependent
-Ensure indwelling catheter or suprapubic catheter is not kinked or blocked
-Remove noxious stimuli if possible
-GTN if BP equal or greater than 160 mmHg
-Morphine
-Transport and Notify

Removal of the noxious stimuli is the preferred management, however as this can be often difficult within the pre-hospital environment, symptomatic management and prevention of cerebrovascular catastrophe is the primary goal.
Move the pt gently and slowly, minimise risk of pressure areas developing and maintain normothermia.

Front 11

Stroke
Definition:

Back 11

CVA or stroke is damage to the brain resulting from disruption of its blood supply. This may be cerebral thrombosis, cerebral embolism or cerebral haemorrhage.

Transient ischaemic Attacks (TIA): is caused by the temporary disturbance of blood supply to a restricted area of the brain, resulting in brief neurologic dysfunction that usually persists for less than 24 hours. Most TIA last for a much shorter period however 5-10% of TIA pts will have a stroke within 2 days.

Front 12

Stroke
Aetiology:

Back 12

Ischaemic Strokes (85%): Inadequate brain perfusion leading to dysfunction & necrosis of the brain tissue in that area. This type of stroke results from thrombosis (obstruction of a blood vessel by a blood clot forming locally), embolism (due to a embolus from elsewhere in the body), systemic hypoperfusion (general decrease in blood supply e.g. in shock) and venous thrombosis..

Haemorrhagic Strokes (15%): Damage to the brain from leakage of blood from vessel, causing local irritation to or destruction of brain tissue. May result from vessel rupture (berry aneurysm) or from a hypertensive episode. Tends to cause more widespread & more severe brain injury, & major bleeds cause immediate raised intracranial pressure & secondary global brain injury from worsening perfusion.

Front 13

Stroke
Pathophysiology:

Back 13

Ischemic stroke occurs due to a loss of blood supply to part of the brain,initiating the ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after a few hours will suffer irreversible injury possibly leading to death of the tissue - infarction. Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of bloodclots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as aconsequence of atria fibrillation, or in the carotid arteries. These break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels.

Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. The pressure may then lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain haemorrhage appears to have direct toxic effects on brain tissue & vasculature

Front 14

Stroke
Signs/Symptoms:

Back 14

Differentiating between the two types of stroke cannot be achieved in the pre-hospital setting, as it requires a CT scan.

Clinical features:
The clinical presentation of a stroke depends on which part of the brain is injured and the extent of the damage.
Strokes may cause:
-Confusion
-Sudden weakness, loss of sensation or movement in part of the body (hemiparesis / hemiplegia)
-Dysphasia
-Dysphagia
-Visual disturbance
-Headache
-Haemorrhagic strokes typically present as a sudden severe headache, ALOC /
unconsciousness, or sudden death

FAST (face, arm, speech, test) Screen
Face – check their face.
Has their mouth drooped?
Arms – Can they lift both arms?
Speech – Is their speech slurred?
Do they understand you?

Front 15

Stroke
Treatment:

Back 15

Use of supplemental oxygen and assisted ventilation is not recommended in patients with Spo2 equal to or greater than 94% because high levels of oxygen are thought to enhance free radical generation and worsen neuronal damage.

Position patient head-up to maximise cerebral perfusion. Avoid jugular vein compression.
-Standard cares
-Oxygen
-IV access
-Antiemetic
-Analgesia
-IV fluid
-Glucose
-Position
-Treat other issues
-Transport and Notify