Neurological Disorders For BSC

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Neurological disorders
For Bsc Nursing Students
JULY,2018
24/10/2023
Objective
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 Describe the causes, pathophysiology, clinical

manifestations, medical ,surgical and nursing
management of :
 Increased intracranial pressure (ICP)
 Seizures/Epilepsy
 Cerebrovascular Disorder(stroke)
 Head injury, Spinal cord injury
 Bell’s palsy(Facial paralysis)
 Parkinson’s diseases, Headache(cephalgia)
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OVER VEIW OF A/P CONT.d
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Cells of the Nervous System

The basic functional unit of the brain is the
Neuron .It is composed of a cell body, a
dendrite, and an axon. ).
Neuroglial cells, another type of nerve cell,
support, protect, and nourish neurons.
Most of brain tumors rises from Glia
cells(45%)
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OVER VEIW OF A/P CONT’d
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CEREBROSPINAL FLUID

CSF, a clear and colorless fluid with a
specific gravity of 1.007,
 Is produced in the ventricles and circulates
around the brain and the spinal cord
through the ventricular system.
 ventricles: the right and left lateral, and the
third and fourth ventricles.
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CEREBRAL CIRCULATION
 The cerebral circulation receives 15% of the
cardiac output, or 750 mL per minute.
 The brain does not store nutrients and has a
high metabolic demand that requires the high
blood flow.
 The brain’s blood pathway is unique because it
flows against gravity;
 Its arteries fill from below and the veins drain
from above
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Increased Intracranial Pressure
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Intra cranial pressure(ICP)

 is the pressure exerted in the cranium by its
contents
 The brain ,Blood, and cerebrospinal fluid(CSF)
 The pressure is measured via the CSF, the normal

pressure of CSF IS 5-15mmHg or 60-
180mmH2O,presssure over 250mmH2O is called
increased ICP,
 Is a symptom of serious underlying disorder.
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Increased Intracranial Pressure cont’
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The rigid cranial vault contains brain tissue

(1,400 g), blood(75 mL), and CSF (75 mL) .
The volume and pressure of these three
components are usually in a state of
equilibrium and produce the ICP.
(ICP=BT+B+CSF)
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Increased Intracranial
9 Pressure cont
 The Monro-Kellie hypothesis states that
because of the limited space for expansion within
the skull, an increase in any one of the components
causes a change in the volume of the others.
 Because brain tissue has limited space to change,
compensation typically is accomplished by
displacing or shifting CSF, increasing the absorption
of CSF, or decreasing cerebral blood volume.
 As ICP increases the complains decreases (as ICP
increases ,compensatory mechanism decreases)
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Increased Intracranial Pressure cont
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 ICP will begin to rise under normal

circumstances in the following conditions
 Minor changes in blood volume and CSF
volume occur constantly due to alterations
in intrathoracic pressure.
 coughing, sneezing, straining, posture,
blood pressure, and systemic oxygen and
carbon dioxide levels.
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Common causes of increased ICP

 Head trauma(injury )
Intracranial hemorrhage,
Hematoma,cerebral edema
 Brain tumors.(increasing tissue volume)
CNS infection eg:meningitis
Brain abscess
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 Increased ICP due to increased CSF volume,

 can result from increased CSF production,
 impaired reabsorption ,
 blocked flow
 Increased ICP caused by increased blood volume results
from Vasodilatation
 The rise in CO2 cause cerebral vasodilatation which
further contribution to a rise in ICP
 Risk factors include any injury or disease to the brain
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Clinical Manifestations
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 change LOC (Early sign )

 Restlessness, confusion, or increasing
drowsiness
 Headache that is constant, increasing in
intensity, and aggravated by movement or
straining.
 Vomiting , papille edema
 Double vision (diplopia)
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Clinical Manifestations
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Vital sign changes are a late indication of Increased

ICP. Cushing’s response is a classic late sign of
increased ICP.
Cushing’s response (or Cushing’s triad) is
Characterized by bradycardia, bradypnea, and arterial
hypertension(increasing systolic blood pressure while
diastolic blood pressure remains the same),
 Widening pulse pressure.
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Clinical Manifestations cont’d
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 Detecting Later Signs of Increased ICP

 LOC continues to deteriorate until the patient is
comatose.
 Altered respiratory patterns develop, including Cheyne-
Stokes breathing
 Projectile vomiting may occur with increased pressure on
the reflex center in the medulla.
 Hemiplegia ( when pressure on the brain stem increases)
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Diagnostic Findings
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 History and physical examination

 computed tomography (CT)scanning
 Magnetic resonance imaging (MRI)
 cerebral angiography
 Skull x ray
 Lumbar puncture is avoided in patients with
increased ICP because the sudden release of
pressure can cause the brain to herniation
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Management
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DECREASING CEREBRAL EDEMA

1,Osmotic diuretics (mannitol) -may be given to
dehydrate the brain tissue and reduce cerebral
edema.
 They act by drawing water across intact membranes,
thereby reducing the volume of brain and
extracellular fluid.
 An indwelling urinary catheter is usually inserted to
monitor urinary out.
2,Corticosteroids (eg, dexamethasone)- help
reduce the edema surrounding brain tumors.
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Management cont’d
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3,Other method for decreasing cerebral

edema is fluid restriction
 Limiting over all fluid intake leads to
dehydration and hemoconcentration

 Hyperventilation of the patient
 Elevating the patient’s head to optimize venous

drainage
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management cont’d
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4.Preventing a Temperature elevation (because fever

increases cerebral metabolism)
 Strategies to reduce temperature
 Include administration of antipyretic medications, ,
and use of a cooling blanket.
5. MAINTAINING OXYGENATION
 Arterial blood gases must be monitored to ensure
that systemic oxygenation remains optimal
 Hyperventilation is recommended
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Management cont’d
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6.MAINTAINING CEREBRAL PERFUSION

 The cardiac output may be manipulated to provide
adequate perfusion to the brain.
 The effectiveness of the cardiac output is reflected in
the cerebral perfusion pressure, which is maintained
at greater than 70 mm Hg .
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Management cont’d
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7 MAINTAINING A PATENT AIRWAY

 Secretions that obstructing the airway must be
suctioned with care
Hypoxia caused by poor oxygenation leads to
cerebral ischemia and edema.
 Coughing is discouraged because coughing and
straining also increase ICP.
 Elevating the head of the bed
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Management cont’d 22
 Proper positioning helps to reduce ICP,The head is

kept in a neutral (midline) position,
 Extreme rotation and flexion of the neck should be
avoided
 Extreme hip flexion is also avoided because this
position causes an increase in intra-abdominal and
intrathoracic pressures
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Management cont’d
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 Stool softeners may be prescribed.

 Abdominal distention, which increases intra-
abdominal and intrathoracic pressure and ICP,
should be noted.
 Suctioning should not last longer than 15 seconds.
 Spacing nursing interventions may prevent transient
increases in ICP.
 Emotional stress and frequent arousal from sleep are
avoided.
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Management cont’d
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Surgical Management
I, REDUCING CSF AND INTRACRANIAL BLOOD
VOLUME
CSF drainage is frequently performed BY
1 An intraventricular catheter
(ventriculostomy),
 When a ventriculostomy or Ventricular catheter
monitoring device is used for monitoring ICP,
 A fine-bore catheter is inserted into a lateral
ventricle of the brain .
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Management cont’d
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Complications of increased intracranial pressure
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1, Brain herniation(is a shifting of brain contents from a

compartment of greater pressure to one of lower pressure
2, Diabetes insipidus,
 is the result of decreased secretion of antidiuretic
hormone.
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SEIZURE DISORDERS
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Episodes of abnormal:
 Motor
 Sensory
or a combination
 Autonomic
 Psychic activity
that result from sudden excessive discharge from
cerebral neurons.
 A part or all of the brain may be involved.
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SEIZURE…
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 Resulting from sudden excessive discharge from

cerebral neurons .
 A part or all of the brain may be involved.
 Most seizures are sudden and transient
 Seizures can develop at any time during a person’s life,
and they can occur at any time.
 A seizure may be a symptom of epilepsy or other
neurological disorders such as a brain tumor or meningitis.
 Epilepsy is a chronic neurological disorder characterized
by recurrent seizure activity
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SEIZURE…
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Classification of seizures based on the international

Seizure classification society.
SEIZURE
Partial Generalized Unclassified
Seizures beginning Involve electrical i. Neonatal seizures

discharges in
Locally(focal seizure)
the whole brain ii. Infantile spasm
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SEIZURE…
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SEIZURE…
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2.Generalized Seizures (convulsive or

nonconvulsive,bilaterally symmetric, without local onset),
Generalized seizures that involve electrical discharges in the whole brain .
Generalized seizures
i. Absence seizures ( petit mal )
ii. Tonic – clonic seizures ( grand mal )
iii. Myoclonic seizures
iv. Clonic seizures
v. Tonic Seizures
vi. Atonic seizures
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SEIZURE…
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Etiology of seizure or risk factors:

 Idiopathic or cryptogenic (70%)
 Genetic factor (Family History) ,
 Developmental defects
 Acquired hypoxemia of any causes, Fever (child
hood),
 vascular insufficiency , Hypertension, stroke
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SEIZURE…
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 CNS infections,
 Metabolic and toxic condition
(Hypoglycemia,Hypocalcemia,Hyponatermia,Renal
failure,Pesticides)
 Head trauma, Neoplasms,
 allergies
 Drugs,Alcohol & others
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SEIZURE…
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1. Partial Seizures (focal seizures)

A. Simple partial seizure
B. Complex partial seizure
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SEIZURE…
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Clinical features
A. Simple Partial Seizures (Older terms for simple partial
seizures include Jacksonian and focal motor.)
 Consciousness is not impaired
 Motor, sensory, autonomic or psychiatric.
 Motor manifestation focal clonic or tonic movement of :
 Angle of mouth may jerky
 Only Finger or hand may shake
 Person s may experience unusual or unpleasant
sights,sounds,odors or tastes
 This seizure activity may spread over one side of the body.
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SEIZURE…C/F
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B. Complex partial seizure

 Impaired consciousness
 Unable to respond appropriately to visual or verbal commands
during the seizure.
 Begins with an aura.(warning sign)
 Start of the ictal phase is often a sudden behavioral arrest or
motionless stare.
Ictal means(seizure)
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SEIZURE…C/F
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PARTIAL SEIZURES. Repetitive, purposeless behaviors,

called automatisms, are the classic symptom of partial
seizures.
Chewing
 lip smacking
 picking movement of the hands
 Staring
 display of emotions.
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SEIZURE…C/F
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Patients may be labeled as mentally ill, particularly if

automatisms include unacceptable social behaviors such
as spitting or fondling themselves
 The patient appears to be in a dreamlike state while
picking at his or her clothing, chewing, or smacking his or
her lips
 Patients are not aware of their behavior or that it is
inappropriate.
Have also post-ictal confusion and transition to full
recovery may take minutes to hours.
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SEIZURE…C/F
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Generalized Seizures
i. Absence seizure (petit mal)
Common in children
 Sudden and brief lapses of consciousness without
loss of postural control.

 Lasts for only few seconds.
 Subtle motor manifestations:
 blinking of the eyes
 chewing movements.
 May occur as many as hundreds of times per day.
 There is no post-ictal confusion.
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SEIZURE…C/F
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 It is usually detected by unexplained daydreaming and

decline in school performance.
 It usually begins in childhood (4-8 yrs), and it often has
a good prognosis,
 With 60-70% of such patients will have spontaneous
remission during adolescence.
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SEIZURE…C/F
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ii. Generalized tonic clonic seizure(Grand mal)

The most common seizure type(60%)
 Ictal phase begins with tonic contraction of muscles throughout
the body:
 Which is responsible for loud moan or cry (due tonic
contraction of the muscles respiration and the larynx)
Tonic posturing
Respiration is impaired
The patient falls to the ground
there may be tongue biting due to tonic contraction of the jaw
muscles.
 Phase of Grand Mal:Aura, epileptic cry ,tonic ,clonic,post
ictal
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SEIZURE…C/F
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 After 10 – 20sec tonic phase evolves to clonic phase

 Clonic phase lasts for another 1 minute
 Characterized by bilateral jerking clonic movement
involving the whole body.
 Contraction with relaxation of major muscles
 The patient is incontinent of urine and stool
 Biting the lips or tongue may cause bleeding.
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SEIZURE…C/F
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SEIZURE…C/F
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iii. Myoclonic seizure
 Sudden and brief muscle contraction
 Involve one part of the body or the entire.

 Can be physiologic or pathologic.
 Is most commonly seen with metabolic
disorders, degenerative diseases of the CNS or
anoxic brain injury.
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SEIZURE…C/F
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iv. Atonic Seizures

 Sudden loss of postural muscle tone, lasting 1 to 2
Seconds.
 Consciousness is briefly impaired
 Usually manifest as a head drop or nodding
movement
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Assessment & Diagnosis
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 DX is aimed at the types of seizure, their

frequency and severity
 Pt’s Hx & P/E.
 History of events
 History of suggesting cause and risk factors
 Eg: factors that precipitate seizure
 Events of pregnancy and child birth
 Mode of delivery ,instrumental delivery ,like vacuum,or forceps
delivery
 History of head injury ,CNS infection
 Neurologic evaluations
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 EEG (Electroencephalography)
 Aids in classifying the types of seizure and the
treatment
 Neuroimaging preferably :MRI,CT scan
 Used to detect lesions in the brain
 Other routine laboratory assessment
 CBC.
 Urinalysis
 Serum glucose(FBS,RBS)
 Liver function test
 RFT
 Electrolytes test
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EEG
A graphic recording of the electrical activity of the
superficial layers of the cerebral cortex.
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EEG
EPILEPSY
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Definition:
It is a group of syndromes characterized by
unprovoked, recurring seizures.
The most common syndromes being those with
generalized seizures and those with partial-
onset seizures.
Epilepsy
Primary Secondary
Idiopathic Symptom of another
underlying condition.
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Epidemiology
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Epilepsy is estimated to affect 0.5-4% of the population

around the world.
The prevalence is said to be higher in developing
countries.
Grand mal seizure account for 40 to 80% of all types of
epileptic seizures.
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Epidemiology cont’d
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In Ethiopia, based on a study done by

Teklehaymanot R. the prevalence of active epilepsy
is estimated to be 5.2/1000.
Analysis of 468 epileptics seen in neurology clinics
of Addis Ababa showed highest incidence in males
aged 11-20 years.
The commonest type of seizure was found to be
grand mal seizure accounting for 60% of all cases.
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It is estimated that 5-10% the population will

have at least one seizure attack in their life time,
with the highest incidence occurring in early
childhood and late adulthood.
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It is estimated that 5-10% the population will have at

least one seizure attack in their life time,
with the highest incidence occurring in early childhood
and late adulthood.
Epilepsy is not associated with intellectual level.
Patient with epilepsy without other brain or
nervous system disabilities fall within the same
intelligence ranges as the overall population.
Epilepsy is not synonymous with mental
retardation or illness.
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THE EPILEPSIES
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is a group of syndromes characterized by recurring

seizures.
Types of epilepsies are differentiated by how the seizure
activity manifests and EEG feature.
the most common syndromes being those with
generalized seizures and those with partial-onset
seizures.
Epilepsy can be primary (idiopathic) or secondary, when
the cause is known
the epilepsy is a symptom of another underlying
condition such as a brain tumor .
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Pathophysiology
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Messages from the body are carried by the neurons

(nerve cells) of the brain by means of discharges of
electrochemical energy that sweep along them.
These impulses occur in bursts whenever a nerve
cell has a task to perform.
Sometimes, these cells or groups of cells continue
firing after a task is finished.
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Etiology
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Causes of seizures cont’d
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can be categorized as
 Idiopathic
 EX- genetic, developmental defects
 acquired.
 hypoxemia of any cause, including vascular insufficiency,
fever (childhood),
 head injury, hypertension, central nervous system
infections,
 metabolic and toxic conditions (eg, renal failure,
hyponatremia, hypocalcemia,hypoglycemia, pesticides),
 brain tumor, drug and alcohol withdrawal, and allergies .
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Etiology of epilepsy/seizure
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or risk factors
 Idiopathic or cryptogenic ;in which the cause is

unknown,accounts for the majority.
 Genetic factor /family history
 Perinatal causes-perinatal asphyxia,birth
trauma,perinatal infection
 CNS infection-meningitis,cerebral
malaria,encephalitis,toxoplasmosis
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CAUSES
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 head injuries, brain tumors ,abscess, and congenital

malformations.
 toxicity (carbon monoxide and lead poisoning)
 circulatory problems-stroke,vascular
malformations, fever,
 metabolic and nutritional disorders, and alcohol
intoxication .
 drugs-theophylline,cocaine,lidocaine.
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Management
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 Treatment of underlying condition
 Avoidance of precipitating factor
 Suppression or control of recurrent seizure
 Antiepileptic drug therapy (AEDT)
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Management
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PHARMACOLOGIC THERAPY
 Many medications are available to control seizures,
although the mechanisms of their actions are still
unknown .
 The objective is to achieve seizure control with
minimal side effects.
 Medication therapy controls rather than cures
seizures.
 Medications are selected on the basis of the type of
seizure being treated and the effectiveness and safety
of the medications .
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Management…
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Medical Management
 To prevent subsequent seizure using a single agent , in
order to limit side effects.

 The drugs should be administered in progressive dose
until seizure control.

 If monotherpay fails, a second drug added to the pt’s
regimen.
 If control is achieved, first agent might be carefully
withdrawn.
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Management…
63
A. Phenobarbitone
In developing countries,
 is the drug of choice for the control of partial and GTC seizures,
due to the wide availability and cheaper cost of the drug
Dosage forms: 15, 30, 60 and 100 mg tabs.
 Starting dose for adults is 60mg PO daily.
 If seizure is not controlled the dosage may be increased gradually.
 If Rx fails or poor control with maximum , tolerable doses, a 2nd
AEDS is often added.
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Management…
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B. Phenytoin:
 Usual prescribed as a 2nd line drug in
resource limited settings.
Dosage:
 100 mg PO BID or TID , which may be gradually
increased to a max of 200 mg PO TID.
Side effects:
• Gingival hyperplasia
• Coarsening of facial feature
• Toxic hepatitis
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Management…
65
Primary GTCS Partial Absence Atypical absence

myoclonic,
Atonic.
First line Valproic acid Carbamazepine Valproic acid Valproic acid.

Lamotrigine Phenytoin Ethusuximide
Valproic acid
Second line Phenytoin Topiramate Lamotrigin Lamotrigin.

Carbamazepine Phenobarbitone. Clonazepam Clonazepam.
Phenobarbitone Topiramate.
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Management…
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Surgical methods
 For patients whose epilepsy results from:
 Intracranial tumors
 Abscesses
 Cysts or
 Vascular anomalies.
 Patient’s who are refractory to medical ,control benefit from
surgery. (intractable seizure disorders that do not respond to
medication
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Management…
67
 Surgical removal of epileptogenic region

 Cutting corpus callosum to prevent spread of seizures b/n
hemispheres
 Temporal lobe resection
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STATUS EPILEPTICUS
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Definition:
 A condition characterized by continuous or repetitive seizure
with impairment of consciousness during interictal period,

which lasts for more than 30 minutes.
 Acute prolonged seizure activity
 Generalized seizures that occurs with out full recovery of
consciousness between attacks

 It is a medical emergency.
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ETIOLOGY
69
Cause or precipitated by:

 Non compliance with AED(with drawls of antisezure medication )
 CNS infections
 Metabolic derangement
 Tumors
 Trauma
 Stroke
 Fever
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CLINICAL FEATURE
70
 Patient is having over convulsion
 After 30-35 min of uninterrupted seizure, the signs may
become increasingly subtle.

DIAGNOSTIC FINDINGS
 EEG
 History of epilepsy /seizure ,withdrawal of the drugs
 Blood tests
 Glucose, Electrolytes, LFT, RFT .
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Complications
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 Hypoxia
 Metabolic acidosis
 Hypotension
 Hyperthermia
 Irreversible neuronal injury
 Hypoglycemia
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MANAGEMENT
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 Goals of treatment:
 To stop the seizures as quickly as possible.
 To ensure adequate cerebral oxygenation
 To maintain the patient in a seizure-free state.
Emergency supportive measures:
 Keep Airway patent and maintain breathing
 Secure IV line and take blood for lab Invn.
 Give glucose IV with Thiamine
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MANAGEMENT
73
Emergency Supportive measures.

 Keep airway patent and maintain breathing.
 secure IV line
 Take blood for laboratory investigation.
2. Control the seizure with anticonvulsant.
Diazepam IV 5-10mgIV.
Phenoytoin 20 mg/min if seizure continues.
General anesthesia with phentobarbitol, if seizure becomes
refractory.
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NURSING M.g. of seizure/epilepsy
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 Areas of the body involved

 Type of movements in the part of the body involved
 Whether the eyes or head turned to one side
 Presence or absence of automatisms
 Incontinence of urine or stool
 Duration of each phase of the seizure
 Unconsciousness, if present, and its duration
 Confused or not confused after the seizure
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NURSING M.g.t…
75
In addition to providing data about the seizure,
nursing care for preventing injury and supporting the

patient physically as well as psychologically
 The circumstances before the seizure (visual, auditory,
or olfactory stimuli, tactile stimuli, emotional or
psychological disturbances, sleep, hyperventilation)
 The occurrence of an aura (visual, auditory, or
olfactory)
 The first thing the patient does in a seizure
 where the movements or the stiffness starts.
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Nursing Management After a Seizure
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 the nurse’s role is to document the events leading

to and occurring during the seizure.
 prevent complications (eg, aspiration, injury).
 To prevent complications,the patient is placed in
the side-lying position .
 if needed to maintain a patent airway.
 The bed is placed in a low position with side rails
up and padded if necessary to prevent patient
injury.
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NURSING M.g.t…
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NURSING M.g.t…
78
After a Seizure
Proper documentation of the events during and
after the seizure to prevent complications.

Patient is placed in the side-lying position.
Seizure precautions are maintained:
 Functioning suction equipment

 Suction catheter and oral airway
 Low position bed with 2 to 3 side rails up and padded.24/10/2023
Nursing Management During a
Seizure
79
 To observe and record the sequence of symptoms.

 The nature of the seizure usually indicates the type of
treatment that is required
 . Inability to speak after the seizure
 Movements at the end of the seizure
 Whether or not the patient sleeps afterward Cognitive status
(confused or not confused) after the seizure
 In addition to providing data about the seizure, nursing care is
directed at preventing injury and supporting the patient.
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Nursing Process cont’d
80
 The patient is encouraged to follow a regular and

moderate routine in life style, diet (avoiding
excessive stimulants), exercise, and rest.
 Some patients’ need to avoid photic stimulation
(bright flickering lights, television viewing). Wearing
dark glasses may help control this problem.
 Tension states (anxiety, frustration) induce seizures in
some patients.
 Because seizures are known to follow alcohol intake,
alcoholic beverages are restricted.
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81
Managing Psychosocial Issues.

 Social stigma: avoid misconceptions in the public through
health education.
 psychiatric problems: depression, psychosis, anxiety
should be treated.
 Social problems: (education ,employment, marriage):
encourage patients to go school/to work,to get married
and establish family.
 Educate patients and families: about the diseases and what
precautions patient should take:
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82
 Avoid alcohol; check with physician before taking

additional prescription or over-the-counter medications.
 Avoid activities that require alertness and coordination
( driving, operating machinery) until after the effects of the
drug have been evaluated. swiming ,climbing the
tree ,riding horse
 Maintain oral hygiene and have regular dental care.
 Carry a personal identification card stating the name of
the drug you are taking.
 regular follow up of the patient
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83
 Keeps laboratory appointment after hospital discharge

serum level determination of antiepileptic drug
 Avoids factors/situations that may precipitate seizures
(flickering light, hyperventilation)
Strives to improve psychosocial adjustment
 Identifies significant other with whom to talk
 Is able to discuss feelings
 Identifies rights under Federal law
24/10/2023
84
Cerbrovascular accident
(Stroke)
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LEARNING OBJECTIVES
85
 To identify the types and causes of stroke.
 Identify clinical manifestations of stroke
 To apply nursing process to develop a plan of care for the
patient experiencing stroke.
24/10/2023
OUTLINE
86
 Definition of stroke
 Etiologic classification of stroke
 Pathophysiology of ischemic stroke(IS)
 Clinical Manifestations IS
 Assessment and Diagnostic Findings of IS.
 Associated risk factors of IS.
 Medical & surgical mgts
 Nursing process of patients with IS.
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LEARNING OBJECTIVES
87
To identify the types and causes of stroke.
Identify clinical manifestations of stroke
To apply nursing process to develop a plan of care for the
patient experiencing stroke.
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Cerebrovascular disorders (stroke)
88
Cerebrovascular disorders (stroke)- term that

refers to any functional abnormality of the
central nervous system (CNS) that occurs
when the normal blood supply to the brain is
disrupted.
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Epidemiology
89
 Stroke is prevalent all over the World wide.

 It is third commonest cause of death in
developed world .
 Following Coronary heart diseases and cancer.
 It is a leading cause of disability.
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Incidence
90
Approximately 500,000 people experience a

new stroke.
 Approximately 160,000 die of a stroke each
year
 The prevalence and incidence of stroke is also
on the rise in developing countries.
24/10/2023
Classification Stroke
91
1, Etiologic classification
can be divided into two major categories:
A, Ischemic stroke -(85%), in which vascular
occlusion and significant hypoperfusion
occur.
It is termed “Brain attack”
Is a sudden loss of function resulting from
disruption of the blood supply to a part of
the brain.
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Ischemic Stroke
92
Are subdivided in to different types

according to their cause:
A,THROMBOTIC(61%)

large artery thrombosis : resulting from
narrowing of cerebral arteries due to
atherosclerosis.
 small penetrating artery thrombosis
Also called lacunar strokes b/c cavity created.

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Ischemic Stroke…
93
B, cardiogenic embolic stroke

 Are associated with cardiac
dysrhythmias,usually atrial fibrillation.
 Emboli originate from the heart and
circulate to the cerebral vasculature.
 Most commonly the left middle cerebral
artery.
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Ischemic Stroke…
94
24/10/2023
Types
Embolic Thrombotic
 Blood clot travels to Blood flow is blocked

the brain to the brain
Ischemic Stroke…
95
C,Cryptogenic and others

 strokes, which have no known cause.
D, Other strokes, can be from drugs - cocaine use,
coagulopathies,
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Ischemic Stroke…
96
24/10/2023
Classification Coverage
1 Small penetrating artery 25%
thrombosis
2 Large artery thrombosis 20%
3 Cardiogenic embolic stroke 20%
4 Cryptogenic 30%
5 Other 5%
Ischemic Stroke…
97
Ischemic Stroke
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Hemorrhagic Stroke
98
B,Hemorrhagic (15%), in which there is extravasation of

blood into the brain.
 caused by an intracranial hemorrhage
Mainly associated with unrecognized or poorly
controlled hypertention.
 subarachnoid hemorrhage.
from ruptured intracranial aneurysm, or certain
medications (eg, anticoagulants and amphetamine)
 Patients generally have more severe deficits and a longer
recovery time compared to those with ischemic stroke .
 is a much common cause of stroke in developing countries
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Stroke…
99
Etiologic classification
Ischemic Hemorrhagic
CAUSES
 Large artery thrombosis

 Intracerebral hemorrhage
 Small penetrating artery  Subarachnoid hemorrhage
thrombosis • Cerebral aneurysm
 Cardiogenic embolic • Arteriovenous malformation
 Accounts  80% - 85%  Accounts  15% - 20%
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H.Strokes…pathophysiology
100
 Depends on the cause and type of cerebrovascular

disorder.
 Hemorrhage, aneurysm, or AVM presses on nearby
cranial nerves or brain tissue causing subarachnoid

hemorrhage.
 ICP resulting from the sudden entry of blood into the
subarachnoid space.
 Brain metabolism is disrupted
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H.Strokes…pathophysiology
101
24/10/2023
Pathophysiology of Ischemic
stroke
102
 Disruption of the cerebral blood flow
 Complex series of cellular metabolic events
 (ischemic cascade)
 Ischemic cascade begins when cerebral blood flow falls
to less than 25 ml/100 g/min.

 At this point, neurons can no longer maintain aerobic
respiration.
 Early in the cascade, an area of low cerebral blood flow
exists around the area of infarction. 24/10/2023

Pathophysiology …
103
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Pathophysiology of stroke…
104
Processes contributing to ischemic brain cell injury.

Courtesy of National Stroke Association,
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2,Classification based on the duration of
stroke
105
A. Transient Ischemic attack: -

 TIAs are focal neurologic deficit lasting < 24hrs
 confined to an area of brain perfused by specific
artery.
 and neurologic deficit resolves in less than 24 hrs.
B. Reversible Ischemic neurologic deficit:

 Sudden onset focal neurologic deficit which lasts
for more than 24hrs,
 but the neurologic deficit recovers/resolves/.
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Classification based on the duration of stroke
106
Stroke in evolution:
 A focal neurologic deficit.
 The degree of which is progressing over a couple of
hours or days.
Complete Stroke:
 Sudden onset of focal neurologic deficit,
 in which the deficit neither improves nor gets worse over
time. It is often associated with infarction of part of the
brain.
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Warning Signs for Stroke
107
Warning Signs
 All patients should be taught to recognize warning signs of a
stroke, and to call 911 immediately if they occur.
 Warning signs include:
 Sudden numbness or weakness of face, arm, or leg(especially
on one side of the body)
 Sudden confusion, trouble speaking, or understanding
 Sudden trouble seeing in one or both eyes
 Sudden trouble walking, dizziness, loss of balance,or
coordination
 Sudden severe headache with no known cause
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Major risk factors associated with stroke include
108
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Clinical Manifestations of stroke
109
 Symptoms are varied and depend on the area of the brain

affected.
 Common symptoms include
 visual disturbances,
 language disturbances,
 weakness or paralysis on one side of the body
 difficulty swallowing (dysphagia).
 In addition, the patient with a hemorrhagic stroke may
experience rapid deterioration, drowsiness, and a
severe headache, often described as “the worst headache of my
life
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Clinical Manifestations of stroke
110
Language Disturbances
Aphasia refers to the absence of language;
Dysphasia refers to difficulty with speech .
Aphasia may be expressive, in which the patient knows
what he wants to say but cannot speak or make sense,
Aphasia may be receptive, with an inability to
understand spoken and/or written words.
Global aphasia occurs when both expressive and
receptive aphasia are present.
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Clinical Manifestations…
111
 Dysarthria is Slurred or indistinct speech and abnormal pronunciation of

words and articulation because of a motor problem
(difficulty in speaking caused by paralysis of the muscles responsible for
producing speech)
 Apraxia (inability to perform a previously learned action)
Motor, sensory, cranial nerve, cognitive, and other functions may be
disrupted.
 MOTOR LOSS
 The most common motor dysfunction is Hemiplegia (paralysis of
one side of the body) due to a lesion of the opposite side of the brain.
 Hemiparesis,or weakness of one side of the body.
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112
24/10/2023
Strokes occur in the brain and
affect the opposite side of the body
113
In the early stage of stroke

Flaccid paralysis
loss of or decrease in the deep tendon
reflexes.
When these deep reflexes reappear (usually
by 48 hours), increased tone with spasticity
of the extremities on the affected side.
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114
SENSORY LOSS(Perceptual Disturbances)

Visual perceptual dysfunctions are due to disturbances
of the primary sensory pathways between the eye
and visual cortex.
Hemianopia (loss of half of the visual field) may
occur from stroke and may be temporary or permanent.
The affected side of vision corresponds to the
paralyzed side of the body.
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115
 The patient's head turns away from the affected side of

his body, and he tends to neglect that side and the space
on that side.
 In such instances, the patient is unable to see food on
half of the tray, and only half of the room is visible.
 Disturbances in visual-spatial relationships (perceiving
relationship of two or more objects In spatial areas)
 are frequently seen in patients with left hemiplegia.
 The patient may not be able to dress himself because of
his inability to match his clothing to his body parts.
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116
Bladder Dysfunction.
After a stroke the patient may have transient
urinary incontinence
due to confusion, inability to communicate his
needs, and inability to use the urinal/bedpan
because of impaired motor and postural controls.
Occasionally after a stroke the bladder becomes
atonic with impaired sensation in response to
bladder filling.
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117
COGNITIVE IMPAIRMENT AND

PSYCHOLOGICAL EFFECTS
 If damage has occurred to the frontal lobe
learning capacity,memory, or other higher cortical
intellectual functions may be impaired.
 manifested by emotional lability, hostility,
frustration, and lack of cooperation.
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118
24/10/2023
Cognitive Deficits
 Short- and long-term memory loss
 Decreased attention span
 Impaired ability to concentrate
 Altered judgment
Diagnosis
119
History and physical examination important

Important historical Information includes:
Mode of onset and pattern of progression.
Embolisms usually occur suddenly when the patient is
awake, most often early in the morning, giving maximum
deficit onset.
Hemorrhagic stokes also occur suddenly while the patient
is awake and may be physically active or straining and
progressive with minutes to hours.
24/10/2023
Diagnosis
120
History and physical examination

Thrombosis often occurs during sleep hour or
present upon arising from bed progressing in
stepwise fashion.
24/10/2023
diagnosis
121
physical examination
 give clue to the type of stroke the patient is suffering from.
Absent/reduced peripheral pulses suggest atherosclerosios
or embolism.
 presence of neck bruit suggests extra cranial occlusion of
carotid arteries.
cardiac abnormalities: such as atrial fibrillation, murmurs
or cardiac enlargement may suggest embolic stroke, the
embolus originating from the heart.
24/10/2023
diagnosis
122
 Ophthalmoscopic examination: Papilledma or retinal

hemorrhage may suggest subarachnoid hemorrhage or
intracranial pressure.
 Fever raises concern for infectious etiologies.
 Increased blood pressure for hypertention.
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Assessment and Diagnostic
Findings
123
24/10/2023
 Careful history and a complete physical and
neurologic exam.
 ECG & carotid ultrasound
 FBS, Lipid profile
 Coagulation profile: to look bleeding tendencies.
Diagnosis
124
Different investigations are needed to confirm the diagnosis.

 Imaging Studies (CT or MRI): are the most important .
 CT can identify or excludes hemorrhagic stroke and other
conditions which stimulate stroke .
 MRI is more sensitive than CT for early diagnosis of brain
infarction
 ECG & carotid ultrasound
 FBS, Lipid profile
 Coagulation profile: to look bleeding tendencies.
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Diagnostic…MRI
125
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Assessment and Diagnostic…CT scan
126
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Diagnostic…
127
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Diagnostic…
128
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Assessment and Diagnostic…
129
Echocardiogram – detects if any thrombus (blood

clot) within the heart chambers
24/10/2023
Other tests are
130
 Lumbar Puncture: - may be needed to make a diagnosis

of small SAH .
 Angiography: to identify the exact location and the
specific artery blocked.
 Echocardiography: to look for cardiac sources of
embolization.
 CBE,ESR, VDRL ,FBS, Lipid profile: to look for
diabetes and hyperlipidemia are risk factors for stroke.
24/10/2023
MANAGEMET OF STROKE
131
Goal of treatment:
 Interruption of further brain damage.
 Managemet of complication.
General Measures
 Admit the patients where close follow up can be given.
 continue follow up and maintenance of vital functions.
 Airway and ventilation.
 Controlling of blood pressure.
 Controlling body temperature.
 Fluid administration/hydration
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MANAGEMET OF STROKE
132
 Adequate oxygenation of blood to the brain is

necessary to minimize cerebral damage.
 Blood pressure and cardiac output must be
maintained to sustain cerebral blood flow, and hydration
(intravenous fluids)
 Oxygen therapy, if necessary, should be given at an
adequate perfusion pressure.
 The patient is placed in a lateral or semiprone position
with the head of the bed slightly elevated to lower
cerebral venous pressure.
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MANAGEMET OF STROKE
133
Endotracheal intubation and mechanical ventilation

are necessary for patients with massive stroke.
The patient is monitored for pulmonary complications
(aspiration, atelectasis, pneumonia), which may be due
to loss of airway reflexes, immobility, or
Hypoventilation.
The heart is examined for abnormalities in size,
rhythm, and signs of congestive failure.
A dysrhythmia may have caused a cerebral embolus and
must be corrected.
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MANAGEMET OF STROKE
134
 If the patient is comatose or has impaired mental status

changing the patients position every 2 hrs and avoid the
occurrence of bed sores.
 bladder and bowel care: if the patient has incontinence-
Inserting catheter.
 Infections such as aspiration pneumonia should be treated
with antibiotics.
24/10/2023
MANAGEMET OF STROKE
135
Management of specific Etiologies

1). Atherosclerotic Stroke (Thrombotic Stroke).
I). Thrombolytic therapy:
thrombolytic therapy with medications such as rt-PA
(plaminogen activator), to patients who present with in 3
hrs of onset of stroke helps to lyse the thrombus and
restore perfusion to the affected brain
24/10/2023
MANAGEMET OF STROKE
136
III, Anti-platelet aggregation agents.

 Aspirin reduces the incidence of stroke and vascular
mortality.
 General recommendation is to give 325 mg of ASA once
daily.
 It may not help to resolve the already formed thrombus,
but ASA prevents recurrence of stroke.
24/10/2023
MANAGEMET OF STROKE
137
Embolic Stroke: (Cardiogenic embolus)

 Anticoagulation is indicated to prevent recurrent embolic
stroke.
 Anticoagulation with heparin should be initiated when the
acute phase of stroke is over.
 Care should be taken to avoid traumatic injury.
 Warfarin is used for chronic anticoagulation.
II, Anticoagulants:
 use of Heparin or Warfarin .
 Low dose heperin can give for prevention of
thromboembolism.
24/10/2023
MANAGEMET OF STROKE
138
Intracerebral hemorrhage
 continue supportive measures.
 control very high blood pressure.
 surgical consultation is indicated for removing cerebelar
hematoma, as it may compress vital centers in the
brainstem.
 If patient is hypertensive
 Short acting antihypertensive drugs are
preferred.hydralizen iv
 Diuretics to reduce cerebral edema.
24/10/2023
MANAGEMENT OF STROKE
139
Subarachnoid Hemorrhage
 supportive measures include bed rest, sedatives,
analgesis, laxative.
 control of hypertension and
 Nifidipin (calcium channel blocker) is given to prevent
neurologic deterioration due to vasopasm.
24/10/2023
MANAGEMET OF STROKE
140
Surgical therapy: Saccular aneurysms are treated

surgically.
Prevention of further stroke:
 control of hypertension.
 control blood sugar in diabetics.
 cessation of smoking.
 physical activity and weight reduction
24/10/2023
MANAGEMET OF STROKE
141
 Anticoagulation for atrial fibrillation.

 ASA 75mg Po daily in individuals older than 50 and have
history of TIA.
 Rehabilitation is very important part of Management, and
it shall be started early and include-
 Physiotherapy
 Occupational and speech therapy.
24/10/2023
142
Assessment
1. A change in the level of responsiveness as evidenced
by movement, resistance to changes of position, and
response to stimulation; orientation to time, place, and
person.
2. Presence or absence of voluntary or involuntary
movements of the extremities; the tone of the muscles;
the body posture; and the position of the head
3. Stiffness or flaccidity of the neck
24/10/2023
143
4. Eye opening, the comparative size of the pupils and

papillary reactions to light, and ocular position
5. The color of the face and the extremities; the
temperature and the moisture of the skin
6. The quality and the rates of pulse and respiration;
arterial blood gases as indicated, body temperature, and
arterial pressure
7. Ability to speak
8. Volume of fluids ingested or administered and the
volume of urine excreted each 24 hours
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144
After the acute phase, the nurse assesses the

following functions: mental status (memory,
attention span, perception, orientation; affect,
speech/language), sensation/perception , motor
control (upper and lower extremity movement);
24/10/2023
Nursing process
145
Nursing Diagnoses
Impaired physical mobility related to hemiparesis, loss
of balance and coordination, spasticity, and brain injury
Pain (painful shoulder) related to hemiplegia and disuse
Self-care deficits (hygiene, toileting, transfers, feeding)
related to stroke squeal
Altered urinary elimination (incontinence) related to
flaccid bladder, instability, confusion, difficulty in
communicating
24/10/2023
Nursing process
146
Altered thought processes related to brain damage,

confusion, inability to follow instruction
Impaired verbal communication related to brain damage
High risk for impaired skin integrity related to
hemiparesis/ hemiplegia, decreased mobility
Altered family processes related to catastrophic illness
and care giving burdens
24/10/2023
Nursing process
147
Planning and implementation

Goals: The major goals of the patient (and family) may
include
improvement of mobility.
avoidance of shoulder pain.
achievement of self-care.
attainment of bladder control.
improvement of thought processes.
24/10/2023
Nursing process
148
Nursing interventions
Improving Mobility: Preventing Deformities. . The arm
tends to adduct (adductor muscles are stronger than
abductors) and to rotate internally.
The elbow and the wrist tend to flex, the affected leg
tends to rotate externally at the hip joint and flex at the
knee, and the foot at the ankle joint supinates and tends
toward plantar flexion
24/10/2023
Nursing process
149
Correct positioning in bed is of prime importance to

prevent contractures;
Measures are used to relieve pressure, assist in
maintaining good body alignment, and prevent compressive
neuropathies.
A bed board under the mattress provides firm support for
the body. The patient should remain flat in bed.
Maintaining the upright position in bed for extended
periods is one of the greatest contributors to hip flexion
deformity.
A footboard may be used at intervals
24/10/2023
Nursing process
150
The patient's position should be changed every 2 hours.

To place a patient in a lateral (side lying) position, a
pillow is placed between the legs before the patient is
turned. The upper thigh should not be acutely flexed.
The patient may be turned from side to side, but the
amount of time spent on the affected side should be
limited because of impaired sensation.
24/10/2023
Nursing process
151
Exercise. The affected extremities are exercised passively and

put through a full range of motion four or five times a day:
To maintain joint mobility
To regain motor control
To prevent development of a contracture in the paralyzed
extremity
To prevent further deterioration of the neuromuscular system,
To enhance circulation.
To prevention venous stasis, which may predispose to
thrombosis and pulmonary embolus.
24/10/2023
Nursing process
152
Achieving Self-Care.
As soon as the patient is able to sit up, he is encouraged
to assist in his personal hygiene.
The first step is to have the patient carry out all self-care
activities on the unaffected side. Such activities as
combing the hair, brushing the teeth, shaving with an
electric razor, bathing, and eating can be carried out with
one hand and are suitable for self-care.
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Nursing process
153
 Improving Family Coping Through Health Teaching.

Members of the patient's family play an important role in
the patient's recovery.
Some type of counseling and support system should be
available to them to prevent the care of the patient from
taking a significant roll on their health and interfering too
radically with their life style
 Home Health Care.
24/10/2023
Nursing process
154
Evaluation
Expected Outcomes
Achieves improved mobility
a. Avoids deformities; absence of contractures and footdrop
b. Participates in prescribed exercise program
c. Achieves sitting balance
d. Increases walking time
e. Uses unaffected side to compensate for loss of function of
hemiplegic side
24/10/2023
HEAD INJURIES
155
Head injury is a broad classification that

includes injury to the scalp,skull, or brain .
Traumatic brain injury is the most serious
form of head injury.
The most common causes of traumatic brain
injury are motor vehicle crashes, violence,
and falls.
24/10/2023
Pathophysiology
156
 Damage to the brain from traumatic injury takes two

forms: primary injury and secondary injury.
 Primary injury is the initial damage to the brain that
results from the traumatic event.
 This may include contusions, lacerations, and torn
blood vessels from impact,
acceleration/deceleration, or foreign object
penetration
 Secondary injury evolves over the ensuing hours and
days after the initial injury and is due primarily to
brain swelling or ongoing bleeding.
24/10/2023
Pathophysiology
157
 An injured brain is different from other injured body

areas due to its unique characteristics.
 It resides within the skull, which is rigid, closed
compartment .
 Thus, any bleeding or swelling within the skull
increases the volume of contents within a container
of fixed size and so can cause increased intracranial
pressure (ICP).
24/10/2023
Pathophysiology
158
 If the increased pressure is high enough, it can cause

a downward or lateral displacement of the brain
through or against the rigid structures of the skull.
 This causes restriction of blood flow to the brain,
decreasing oxygen delivery and waste removal.
 Cells within the brain become anoxic and cannot
metabolize properly, producing ischemia, infarction,
irreversible brain damage, and eventually brain
death.
24/10/2023
HEAD INJURIES cont’d
159
SCALP INJURY
 Isolated scalp trauma is generally classified as a
minor head injury.
 Because its many blood vessels constrict poorly, the
scalp bleeds aprofusely when injured.
 Trauma may result in an abrasion , contusion,
laceration, or hematoma beneath the layers of tissue
of the scalp (subgaleal hematoma).
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160
Diagnosis
 P/E--inspection, and palpation.
 Scalp wounds are potential portals of entry of organisms that
cause intracranial infections.
 Therefore, the area is irrigated before the laceration is sutured
 To remove foreign material and to reduce the risk for
infection.
 Wound dressing
 Oral antibiotic drug
 Subgaleal hematomas (hematomas below the outer covering
of the skull) usually absorb on their own and do not require
any specific treatment.
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161
SKULL FRACTURES
 A skull fracture is a break in the continuity of the
skull caused by forceful trauma.
 It may occur with or without damage to the brain.
 Skull fractures are classified as linear, depressed,and
basilar.
 A fracture may be open, indicating a scalp laceration
or tear in the dura .
 closed, in which the dura is intact .
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162
 Simple linear fracture-this is aline of fracture which

usually marks of severe forces of injury.
 Constitute about 80% of all fractures of the skull
 Can be left as such if they are closed
 No specific neurological management is required.
Depressed skull fructure
 This types of fracture is usually as result of blunt
trauma.
 It could be open or closed.
 50|% occurs in frontal area
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163
 The open type of fracturẹ/compound depressed

fracture/has a high risk of infection so that it should
be handled as emergency.
 The depressed fragments may lacerate the dura and
brain tissue.
 In infants: ping-pong fracture, skull deformed but
not broken and should be elevated
Treatment
 Debride and irrigate contaminated wounds
 Full course of interavenouse antibiotics.
 Elevation if indicated
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164
Fractures of the base of the skull

 Tend to traverse the paranasal sinus of the frontal bone or
the middle ear located in the temporal bone; thus, they
frequently produce
 Hemorrhage from the nose, the pharynx, or the ears,
 Blood may appear under the conjunctivae.
 An area of ecchymosis. or bruising, may be seen over the
mastoid (Battle's sign).
 The escape of CSF from the ears (CSF otorrhea) and the
nose (CSF rhinorrhea) suggests basal skull fracture.
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165
 A halo sign (a blood stain surrounded by a yellowish

stain) may be seen on bed linens or the head
dressing and is highly suggestive of a CSF leak.
 Drainage of CSF is a serious problem because
meningeal infection can occur if organisms gain
access to the cranial contents through the nose, ear,
or sinus through a tear in the dura.
 Bloody CSF suggests a brain laceration or contusion.
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Assessment and Diagnostic Findings
166
 History and physical examination

 A computed tomography (CT) scan
 Skull x-rays.
 Magnetic resonance imaging (MRI)
 Cerebral angiography
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Treatment of basal skull fracture
167
 The nasopharynx and the external ear should be kept clean.

 Usually a piece of sterile cotton is placed loosely in the ear,
or a sterile cotton pad may be taped loosely under the nose
or against the ear to collect the draining fluid.
 The patient who is conscious is cautioned against sneezing
or blowing the nose.
 The head is elevated 30 degrees to reduce ICP and promote
spontaneous closure of the leak .
 Persistent CSF rhinorrhea or otorrhea usually requires
surgical intervention.
 IV Antibiotic to prevent infection
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Brain Injury
 The most important consideration in any head injury
is whether or not the brain is injured.
 The brain cannot store oxygen and glucose to any
significant degree.
 Because the cerebral cells need an uninterrupted
blood supply to obtain these nutrients, irreversible
brain damage and cell death occur when the blood
supply is interrupted for even a few minutes.
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Concussion
 A cerebral concussion after head injury is a temporary
loss of neurologic function with no apparent structural
damage.
 A concussion generally involves a period of
unconsciousness lasting from a few seconds to a few
minutes.
 The jarring of the brain may be so slight as to cause only
dizziness and spots before the eyes , or it may be severe
enough to cause complete loss of consciousness for a time.
 If the brain tissue in the frontal lobe is affected, the patient
may exhibit bizarre irrational behavior.
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 The patient may be hospitalized overnight for

observation or discharged from the hospital in a
relatively short time after a concussion.
 Treatment
 involves observing the patient for headache,dizziness,
lethargy, irritability, and anxiety.
 The occurrence of these symptoms after injury is
referred to as postconcussion syndrome.
 Giving the patient information, explanations, and
encouragement may reduce some of the problems of
postconcussion syndrome.
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Contusion
 Cerebral contusion is a more severe injury in which the
brain is bruised, with possible surface hemorrhage.
 The patient is unconscious for more than a few seconds or
minutes.
Clinical signs and symptoms
 depend on the size of the contusion and the amount of
associated cerebral edema.
 The patient may lie motionless,with a faint pulse, shallow
respirations, and cool, pale skin.
 Often there is involuntary evacuation of the bowels and the
bladder.
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 The blood pressure and the temperature are

subnormal, similar to that of shock.
 In general, patients with severe brain injury who
have abnormal motor function, abnormal eye
movements, and elevated ICP have poor outcomes
 Reading assignment
 Admission criteria for head injury
 Classification of severity of head injury based
Glasgow coma scale(GCS)
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Intracranial Hemorrhage
 Hematomas (collections of blood) that develop
within the cranial vault are the most serious brain
injuries.
 A hematoma may be epidural (above the dura),
subdural (below the dura), or intracerebral (within
the brain) .
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Epidural Hematoma /Extradural Hematoma

 After a head injury, blood may collect in the epidural
(extradural) space between the skull and the dura.
 This often results from fractures of the skull that cause
rupture or laceration of the middle meningeal artery,
which runs between the dura and the skull located just
inferior to a thin portion of temporal bone; hemorrhage
from this artery causes pressure on the brain.
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 The symptoms are caused by the expanding

hematoma.
 There is usually a momentary loss of consciousness at
the time of injury
 Followed by an interval of apparent recovery (lucid
interval).
 During the lucid interval, compensation for the
expanding hematoma takes place by rapid
absorption of CSF and decreased intravascular
volume,.
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signs of compression appear

 Usually deterioration of consciousness
 Focal neurologic deficits such as
 Dilation and fixation of a pupil
 Paralysis of an extremity, and the patient
deteriorates rapidly.
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Management.
 An epidura! hematoma is considered an extreme
emergency, as marked neurologic deficit or even
cessation of breathing may occur within minutes.
 The treatment consists of making openings through the
skull (burr holes), removing the clot, and controlling
the bleeding point.
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Subdural Hematoma
 A subdural hematoma is a collection of blood between the dura and the
underlying brain.
 The most common cause is trauma, but it may also occur in case aneurysms.
 A subdural hematoma may be acute, subacute, or chronic, depending on the
size of the involved vessel and the amount of bleeding present.
 Acute subdural hematoma :with in 48 hours after injury
 Sub acute subdural hematoma with in 2 to 14 days injury
 Chronic subdural hematoma: greater than 14 days
 Acute subdural hematomas are associated with major head injury involving
contusion or laceration.
 Usually the patient is comatose, and the clinical signs are similar to those of
epidural hematoma.
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 A rising blood pressure with slowing of pulse and

respirations indicates a rapidly increasing hematoma.
 The mortality rate for patients with acute subdural
hematomas is high, because frequently there is associated
brain damage.
 If the patient can be transported rapidly to the hospital, an
immediate craniotomy is performed to open the dura,
allowing for the solid subdural clot to be evacuated.
 Successful outcome also depends on the control of ICP
and careful monitoring of respiratory
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 patient's clinical signs and symptoms fluctuate.

 There may be severe headache, which tends to come and
go.
 Alternating focal neurologic signs
 Personality changes
 Mental deterioration
 Focal seizures. Unfortunately, the patient may be labeled
neurotic or psychotic if the cause of the symptoms is
overlooked.
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 The treatment of a chronic subdural hematoma

consists of surgically evacuating the clot by
suctioning or irrigating the area.
 The procedure may be carried out through multiple
burr holes.
 craniotomy may be performed for a sizable subdural
mass lesion that cannot be drained through burr holes.
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Intracerebral Hemonhage/Hematoma
 Intracerebral hemorrhage is bleeding into the
substance of the brain.
 It is commonly seen in head injuries in which force is
exerted to the head over a small area ( bullet wounds;
stab injury).
 These hemorrhages within the brain may also result
from systemic hypertension,
 from rupture of a saccular aneurysm;
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 from vascular anomalies;

 from intracranial tumors;
 from systemic causes, including bleeding disorders such
as leukemia, hemophilia, and thrombocytopenia;
 from complications of anticoagulant therapy.
Medical therapy involves
 Careful administration of fluids and electrolytes,
 Antihypertensive medications
 Control of ICP, and supportive care.
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Surgical intervention by craniotomy or

craniectomy permits removal of the blood clot
and provides opportunity for control of the sites
of hemorrhage .
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Nursing Process
185
The Patient With a Head Injury

Assessment
 The health history may include the following questions:
 At what time did the injury occur?
 What caused the injury? An object striking the head?
A fall?
 What was the direction and force of the blow?
 Was there a loss of consciousness?
 What was the duration of the unconscious period?
Could the patient be aroused?
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186
 A history of unconsciousness or amnesia after a head

injury indicates a significant degree of brain damage.
 Assessment of Level of Conscious
ness/Responsiveness.
 Glasgow Coma Scale, which is based on three aspects of
the patient's behavior
 Eye opening
 Verbal responses
 Motor responses to a verbal command or painful stimulus
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188
 vital signs are monitored at frequent intervals to assess the

intracranial status.
 Signs of increasing ICP include slowing of the pulse, increasing
systolic pressure, and widening pulse pressure.
 As brain compression increases, the vital signs tend to be
reversed—the pulse and respiration become rapid, and the
blood pressure may decrease.
 A rapid rise in body temperature is regarded as unfavorable,
because hyperthermia increases the metabolic demands of the brain.
 Tachycardia and arterial hypotension may indicate that bleeding
is occurring somewhere in the body.
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189
Nursing Diagnoses
 Ineffective airway clearance and ventilation related to
hypoxia
 Fluid volume deficit related to disturbances of
consciousness and hormonal dysfunction
 Altered nutrition, less than body requirements, related
to metabolic changes, fluid restriction, and inadequate
intake
 High risk for violence (self-directed and directed to
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Nursing Process
190
 Altered thought processes (deficits in intellectual

function, communication, memory, information
processing) related to results of head injury
 Potential for ineffective family coping related to
unresponsiveness of patient, unpredictability of outcome,
prolonged recovery period, and patient's residual physical
and emotional deficit
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191
Planning
 Goals: The patient's goals may include
 Attainment of a patent airway
 Achievement of fluid and electrolyte balance
 Achievement of adequate nutritional status
 Prevention of injury
 Improvement of cognitive function,
 Accomplishment of effective family coping behaviors.
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Nursing Interventions
Airway Maintenance.
 Keep the unconscious patient in a position that
facilitates drainage of oral secretions, with the head of
the bed elevated about 30 degrees to decrease
intracranial venous pressure.
 Establish effective suctioning procedures- (Pulmonary
secretions produce coughing and straining, which increase
ICP.)
 Monitor the patient on mechanical vent
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193
 Prevention of Injury.
 Environmental stimuli should be kept to a minimum by
keeping the room quiet, limiting visitors, speaking calmly, and
providing frequent orientation information (e.g., explaining
where the patient is and what is being done).
 Adequate lighting may prevent visual hallucinations.
 The patient's sleep-wake cycles should not be interrupted.
 The skin is lubricated with oil or emollient lotion to prevent
irritation due to rubbing against the sheet.
 Improved Cognitive Functioning.
 Patient and Family Education.
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Evaluation
Expected Outcomes
 1. Attains/maintains effective airway clearance,
ventilation, and brain oxygenation
 2. Achieves satisfactory fluid and electrolyte balance
 3. Attains adequate nutritional status
 4. Avoids injury
 5. Shows cognitive progression
 6. Family members demonstrate adaptive coping
mechanisms.
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Bell’s palsy (facial paralysis)
Facial Paralysis(Bell’s palsy)

195
 Bell’s palsy (facial paralysis)

 Is a paralysis of the facial nerve (cranial nerve VII)
 Is due to unilateral inflammation of the seventh cranial
nerve, which results in weakness or paralysis of the facial
muscles on the affected side .
The cause is unknown
 Possible causes may include
 vascular ischemia,(stroke,hypertension)
 viral disease ( HIV/AIDS .Herpes simplex, Herpes
zoster),
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 Autoimmune disease, or a combination of all of these

factors.
 Loss of motor control generally occurs on one side of the
face;
 Bilateral facial palsy occurs in less than 1% of cases.
 Contracture of facial muscles may occur if recovery is
slow.
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Prevalence
 Men and women are affected equally.
 Bell’s palsy is more common in the third trimester of
pregnancy,
 in individuals with immune disorders such as HIV
infection, and individuals with diabetes. Hypertension
 It occurs in all ages (including children) and at all times
of the year.
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Signs and Symptoms

 Onset of symptoms may be sudden or may progress over
a 2- to 5-days period.
 The severity of the paralysis usually peaks within several
days of onset of symptoms.
 Pain behind the ear may precede the onset of facial
paralysis.
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 The patient may be unable to close the eyelid,

 Un able to wrinkle the forehead, smile, raise the eyebrow,
or close the lips effectively.
 The mouth is pulled toward the unaffected side
 Other vague initial symptoms are dry eye or tingling
around the lips with progression to the more recognizable
symptoms .
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 Drooling of saliva occurs, and the affected eye has

constant tearing.
 Sense of taste is lost over the anterior two-thirds of the
tongue.
 Speech difficulties are present.
 Fifty percent of these patients will have complete
recovery in a short period of time.
 Thirty five percent will have full recovery in less than 1
year
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202
 Diagnostic Tests
 History of the onset of symptoms is used to diagnose
Bell’s palsy.
 Observation of the patient confirms the diagnosis.
 An EMG may be done. Predicts level of expected
recovery
 The possibility of a stroke must be ruled out.
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 Therapeutic Interventions
 Prevention of complications is the goal of treatment.
 Prednisone may be given over 7 to 10 days to decrease
edema.
 Analgesics are given for pain control.
 Antiviral medication may be prescribed
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 Moist heat with gentle massage to the face and ear also
eases pain.
 Use of a facial sling aids in eating and supports facial
muscles.
 To reduce pain and prevent muscle atrophy.
 Provide warm, moist compresses prn.
 Massage face.
 Assist with facial exercises several times a day.
 Provide frequent mouth care
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Complications associated with Bell's palsy

include
 facial weakness
 facial spasm with contracture,
 corneal ulceration,
 blindness
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Parkinson’s Disease
206
 Parkinson’s disease is a chronic degenerative movement

disorder that arises in the basal ganglia in the cerebrum.
 It usually begins in the fourth or fifth decade of life, with
symptoms becoming progressively worse as the patient
ages.
 The disease is characterized by tremors, changes in
posture and gait, rigidity, and slowness of movements.
 Approximately 1% of people over 65 have a diagnosis of
Parkinson’s disease.
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208
 Pathophysiology
 The substantia nigra is a group of cells located within the
basal ganglia, which is situated deep within the brain.
These cells are responsible for the production of
dopamine, an inhibitory neurotransmitter.
 Dopamine facilitates the transmission of impulses from
one neuron to another.
 Parkinson’s disease is caused by destruction of the cells of
the substantia nigra, resulting in decreased dopamine
production.
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 Loss of dopamine function results in impairment of

semiautomatic movements.
 Parkinson’s disease is sometimes referred to as an extrapyramidal
disorder because the extrapyramidal tracts that contain motor
neurons are affected.
 Acetylcholine, an excitatory neurotransmitter, is secreted
normally in individuals with Parkinson’s disease.
 The normal balance of acetylcholine and dopamine is interrupted
in these patients, causing a relative excess of acetylcholine,
 which results in the tremor, muscle rigidity, and bradyakinesia
and loss of muscle movement) characteristic of Parkinson’s
disease.
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 Clinical Manifestations
 has a gradual onset and symptoms progress slowly .
 The three cardinal signs are tremor, rigidity, and
bradykinesia(abnormally slow movements).
 Other features include hypokinesia, gait disturbances, and
postural instability
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TREMOR
 resting tremor is present in 70% of patients at the time of
diagnosis.
 Resting tremor characteristically disappears with
purposeful movement but is evident when the extremities
are motionless.
 The tremor may present as a rhythmic, slow turning
motion of the forearm and the hand and a motion of the
thumb against the fingers as if rolling a pill.
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 Tremor is present while the patient is at rest; it increases

when the patient is walking, concentrating, or feeling
anxious.
 RIGIDITY
 Resistance to passive limb movement characterizes
muscle rigidity.
 Passive movement of an extremity may cause the limb to
move in jerky increments referred to as cog wheeling.
 Stiffness of the neck, trunk, and shoulders is common.
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 BRADYKINESIA
 One of the most common features of Parkinson’s disease
is bradykinesia.
 Patients take longer to complete most activities and have
difficulty initiating movement, such as rising from a
sitting position or turning in bed.
 Hypokinesia (abnormally diminished movement) is also
common and may appear after the tremor.
 the patient tends to shuffle and exhibits a decreased arm
swing.
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 the patient develops dysphagia, begins to drool, and is at

risk for choking and aspiration.
 The patient commonly develops postural and gait
problems.
 There is a loss of postural reflexes, and the patient stands
with the head bent forward and walks with a propulsive
gait. The posture
 is caused by the forward flexion of the neck, hips, knees,
and elbows. The patient may walk faster and faster, trying
to move the shuffling gait
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 Assessment and Diagnostic Findings

 History and neurologic examination
 Laboratory tests and imaging studies are not helpful in the
diagnosis of Parkinson’s disease,
 Evaluating levodopa (precursor of dopamine) uptake and
conversion to dopamine in the corpus striatum
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Treatment is directed at controlling symptoms

maintaining functional independence because
there are no medical or surgical approaches that
prevent disease progression.
 Care is individualized for each patient based on
presenting symptoms and social,occupational,
and emotional needs.
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Therapeutic Interventions
There is no cure for Parkinson’s disease. Treatment is aimed
at controlling symptoms and maximizing the patient’s func-
tional level.
Anticholinergic
Blocks the action of acetyl-choline to control
tremor and salivation
Dopamine Agonists Convert into dopamine in the brain
Levodopa/carbidopa combination .
Carbidopa prevents peripheral breakdown of levodopa so more
is available in the CNS
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 Complications
 The most typical acute complications of Parkinson’s
disease
 patients are very prone to falls, which may result in
injuries
 Constipation is common because of decreased activity,
diminished ability to take in food and fluids, and side
effects of anticholinergic medications.
 Patients are encouraged to increase fiber and fluids in
their diet.
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 Treatment is based on a combination of the following:

 (a) Drug therapy.
 (b) Physical therapy.
 (c) Rehabilitation techniques.
 (d) Patient and family education.
 (2) Encourage patient to participate in physical therapy
and an exercise program to improve coordination and
dexterity.
 (a) Emphasize importance of a daily exercise program.
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 b) Instruct patient in postural exercises and walking techniques to

offset shuffling gait and tendency to lean forward.
 (c) Encourage warm baths and showers to help relax muscles and
relieve spasms.
 (3) Instruct patient to establish a regular bowel routine with a
high fiber diet and plenty of fluids.
 Constipation is a problem due to muscle weakness, lack of
exercise, and drug effects.
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 Eat a well-balanced diet. Nutritional problems develop

from difficulty chewing and swallowing and dry mouth
from medications.
 Encourage patient to be an active participant in his/her
therapy and in social and recreational events, as
Parkinsonism tends to lead to withdrawal and depression
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Spinal Cord Injury
223
 Spinal cord injuries

 Excessive force exerted on the spinal column can result in
extreme flexion, hyperextension, compression or rotation.
Etiology
 Motor vehicle accidents(which account for 35% of the
injuries)
 Falls(19%)
 Acts of violence(30%)
 Sports injuries(8%)
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Spinal Cord Injury
224
 The predominant risk factors for Spinal cord injury

include
 Age, gender, and alcohol and drug use.
Individuals at risk for spinal cord injury injuries
 Young adults b/n 15 – 30 yrs of age
 Motor cyclists
 Sky dive
 Foot ball players
 Police & military personnel
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Spinal Cord Injury
225
 The vertebrae most frequently involved in Spinal

cord injury are the 5th, 6th, and 7th cervical (neck),
the 12th thoracic, and the 1st lumbar vertebrae
 There is a greater range of mobility in the
vertebral column in these areas
 Spinal cord injury can be due to cord compression
by bone displacement, interruption of blood supply
to the cord or traction resulting from pulling on the
cord.
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Spinal Cord Injury
226
 Pathophysiology
 Damage to the spinal cord ranges from transient
concussion (from which the patient fully recovers) to
contusion, laceration, and compression of the cord
substance (either alone or in combination)
 Spinal cord injury is can be separated into two categories:

primary injuries and secondary injuries .
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Spinal Cord Injury
227
 Primary injuries are the result of the initial insult or

trauma and are usually permanent.
 Secondary injuries are usually the result of a contusion or
tear injury ,in which the nerve fibers begin to swell and
disintegrate.
 A secondary chain of events produces ischemia, hypoxia,
edema, and hemorrhagic lesions, which in turn result in
destruction of myelin and axons, thought to be reversible
4 to 6 hours after injury.
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Spinal Cord Injury
228
Classification
Spinal cord injuries are classified by
Degree of injury
Level of injury
Mechanism of injury
Neurologic level refers to the lowest level at which
sensory and motor functions are normal.
Below the neurologic level, there is total sensory
and motor paralysis
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Spinal Cord Injury
229
The degree of spinal cord injury

 A complete spinal cord injury means that there is no motor or
sensory function below the level of the injury.
 An incomplete lesion means that there is some function remaining.
 Incomplete spinal cord lesions are classified according to the area
of spinal cord damage: central, lateral, anterior, or peripheral
 This does not necessarily mean that the remaining function will be
useful to the patient.
 Some patients find that having areas where sensation is intact may
be more painful than useful.

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Spinal Cord Injury
230
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Spinal Cord Injury
231
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Spinal Cord Injury
232
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Spinal Cord Injury
233
 The level of injury may be

 Cervical - thoracic or lumbar level
 The cervical and lumbar portions of the spine are
injured more often than the thoracic or sacral segments.
 This is because the cervical and lumbar areas are the
most mobile portions of the spine
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Spinal Cord Injury
234
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Spinal Cord Injury
235
the major mechanisms of injury are

 Hyperextension injury
 Hyper flexion injury
 Compression
 Excessive rotation
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Spinal Cord Injury
236
Signs and Symptoms

Cervical Injuries
Signs and symptoms depend on the level of cord that is
damaged
 Cervical cord injuries can affect all four extremities,
causing paralysis and paresthesias
Impaired respiration, and loss of bowel and bladder
control.
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Spinal Cord Injury
237
 Paralysis of all four extremities is called quadriplegia;

 weakness of all extremities is called quadriparesis
 Injury of the spinal cord at the cervical level results in
quadriplegia(tetraplagia)
 Is the most dangerous and usually results in respiratory
muscle paralysis
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Spinal Cord Injury
238
 If the injury is at C3 or above, the injury is usually fatal

because muscles used for breathing are paralyzed
 An injury at the fourth or fifth cervical vertebra affects
breathing and may necessitate some type of ventilatory
support.
 Narcotic should not be given as analgesic for patients
with high cervical injury
 These patients typically need long-term assistance with
activities of daily living
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Spinal Cord Injury
239
Thoracic and Lumbar Injuries

 Thoracic and lumbar injuries affect the legs, bowel, and bladder.
 Paralysis of the legs is called paraplegia;
 weakness of the legs is called paraparesis.
 Injury of the spinal cord at the thoracic and lumbar vertebral level
can cause paraplegia
 Sacral injuries affect bowel and bladder continence and may
affect foot function.
 Individuals with thoracic, lumbar, and sacral injuries can usually
learn to perform activities of daily living independently.
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Spinal Cord Injury
240
Spinal Shock(neurogenic shock )

 Spinal cord injury has a profound effect on the autonomic
nervous system.
 Immediately following injury, the cord below the injury
stops functioning completely.
 This causes a disruption of sympathetic nervous system
function, resulting in vasodilation, hypotension, and
bradycardia ,paralytic ileus(occasionally),flaccid paralysis
,loss of reflex
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Spinal Cord Injury
241
 Dilation of the blood vessels allows more blood flow just

under the skin.
 This blood cools and is circulated throughout the body,
causing hypothermia.
 Keep the patient covered as much as possible but avoid
overheating.
 In addition, all reflexes below the level of the injury are
lost, and retention of urine and feces occurs.
 Spinal shock can last from a week to many weeks in some
patients.
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Spinal Cord Injury
242
Autonomic dysreflexia or hyperreflexia is usually seen in

injuries above the level of the sixth thoracic vertebra
 Occurs after spinal shock has completed
 Results from uninhibited sympathetic discharge and no
longer controlled by higher centers in the cerebral cortex
 Is characterized by severe hypertension ,brady
cardia,flushing above level of lesion ,severe throbbing
head ache ,nasal stiffness, sweating ,nausia.
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Spinal Cord Injury
243
 Diagnostic test
 History and Complete neurological exam
 Assessment of motor system.
 Motor examination: Check for weakness of muscle power
and tendon reflexes
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Spinal Cord Injury
244
 Assessment of sensory system.

 Assessment of Sensory Examination includes:
 Pain and temperature (by spinothalamic tract).
 Position and vibration (by posterior column tract)
 Light touch.
 Two-point discrimination
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Spinal Cord Injury
245
 Assessment of the reflexes.

 Hematology - electrolyte, glucose, Hgb levels
 X – ray of the Spinal cord – in different positions
 U/A
 CT scan, MRI.
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Spinal Cord Injury
246
 Therapeutic mg’t
 Emergency mg’t
 The initial goals are to sustain life & prevent cord damage
 Secure the airway, breathing and circulation (ABC rule of trauma
management
 Monitor air way have airway equipment available.
 IV resuscitation should be started in patients with spinal shock
 Patients with injuries above C4–5 have some degree of
respiratory impairment.
 The patient may require a tracheotomy and continuous
mechanical ventilation
24/10/2023
Spinal 247
Cord Injury
 Some patients are able to breathe by using a phrenic nerve
stimulator
 Immobilization of vertebral column by skeletal traction.
 Administration of 02
 Maintenance of heart rate ( eg. Atropine ) and B/P (e.g.
Dopamine )
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Spinal Cord Injury
248
 Steroid( prednisone) therapy to reduce edema

 Assess for other injuries and control external bleeding
 Indwelling urinary catheter insertion
 Moderate fluid restriction for the 1st 72 hrs
 Monitor V/S, level of consciousness, 0 2 saturation, cardiac
rhythm(ECG)
 Mgt & attachment to suction intubation
 keep warm.
 Giving Enema
 insertion of Nasogastric tube
24/10/2023
Spinal Cord Injury
249
Bed sore prevention by bed care and frequent position

change
Neurologic damage is prevented by suitable reduction
and immobilization any fracture
Cervical spine malalignment –traction using skull tongs
or a hole apparatus
Open reduction if traction fails
Thoracic and lumbar spine –usually require a plastic body
jacket or plastic cast for three months
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Spinal Cord Injury
250
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Spinal Cord Injury
251
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Spinal Cord Injury
252
Surgery: If there is deterioration of neurological function

after initial assessment
In ability to reduce the fracture or dislocation
Chronic pt Mg’t
 Stress ulcer prophylaxis
 Physical therapy ( range of motion exercise) occupational
therapy ( splints, activities of daily living training )
 Rehabilitation is directed to wards self care and
vocational readjustment
24/10/2023
Spinal Cord Injury
253
Complications
Infection
Impaired respiratory effort, decreased cough, mechanical
ventilation,
immobility all predispose the cervical cord injured patient
to pneumonia.
Catheterization, whether indwelling or intermittent, places
patients at risk for urinary tract infection.
24/10/2023
Spinal Cord Injury
254
 Orthostatic Hypotension
Most spinal cord injured patients no longer have muscular
function in their legs to promote venous return to the
heart.
They also have impaired vasoconstriction.
This leads to pooling of the blood in the legs when the
patient moves from a supine to a sitting position.
If the movement is sudden, the patient may become dizzy
or faint.
24/10/2023
Spinal Cord Injury
255
 Skin Breakdown
Development of pressure ulcers can lead to infection and
loss of skin, muscle, or bone. Treatment of
pressure ulcers is time consuming and expensive
Renal Complications
Urinary tract infections are an ongoing concern to spinal
cord–injured patients.
Both urinary reflux and untreated urinary tract infections
can cause permanent damage to the kidneys.
24/10/2023
Spinal Cord Injury
256
Deep Vein Thrombosis

Lack of movement in the legs inhibits normal blood
circulation.
 Depression and Substance Abuse
Patients with spinal cord injury have a higher than average
incidence of depression and substance abuse
24/10/2023
Head Aches(Cephalgia)
257
 HEADACHES(Cephalgia)
 is one of the t most common of all human physical complaints.
 Head ache is actually a symptom rather than a disease entity
 It is a symptom of underlying disease
As many as 90% of individuals have at least one episode of
headache per year.
 Most headaches are transient events and do not indicate a serious
pathological condition.
 If headaches are recurrent, persistent, or increasing in severity,
the patient should undergo a neurological evaluation.
24/10/2023
258
There are types of head ache

A primary headache is one for which no organic cause can
be identified.
These types of headache include Migraine, Tension type,
and Cluster headaches, Cranial arthritis
A secondary headache is a symptom associated with an
organic cause, such as a brain tumor or an aneurysm.
24/10/2023
259
Headache assessment
Headache characteristics – time of onset, location, frequency,
duration, quality , intensity ,paths of radiation etc
Presence of localized tenderness
Presence of an aura
Associated symptoms occurring before, during or after a
headache
precipitating factors
Activities of daily living patterns
Drug history
Any family history
24/10/2023
260
 Tension or Muscle Contraction Headaches

 The most common type of head ache
 Clinical feature
 Tension headache is characterized by mild or moderate,
bilateral pain.
 Headache is a constant, tight, pressing or band like may
be described as “a weight on top of my head.
 Pain sensation in the frontal, temporal, parietal area or
Occipital
24/10/2023
261
 precipitating factors that may cause tension headache

Including.
 Stress – usually occurs in the afternoon after long
stressful work hours
 Over work
 Sleep disturbance
 Uncomfortable stressful position and/or bad posture
 Hunger (Irregular meal time)
 Eye strain resulting from continuous TV watching,
working on computer screen for a long time.
24/10/2023
262
 Tension head ache Usually lasts less than 24 hrs but can
persist for days or weeks.
Prodromal symptoms are absent, some patients have neck, jaw
discomfort.( there is no nausea and vomiting)
Pharmacotherapy
Non narcotic analgesics(NSAIDS)
Diclofenac , ASA, Ibuprofen, and paracetamol
supportive treatment:
Include the use of relaxation techniques,, rest, localized heat
application, appropriate counseling ,massage of the affected
muscles
24/10/2023
263
 Migraine Headache
 Migraine headache is a benign and episodic disease,
characterized by
 headache, nausea, vomiting and/ or other symptoms of
neurological dysfunction.
 It is the most common cause of vascular headache.
 It approximately affects 15% of women and 6% men.
 It usually begins in childhood or young adult life.
 Family history can be found in 65% of the patient
24/10/2023
264
 PATHOPHYSIOLGY
 A migraine headache is believed to be caused by cerebral
vasoconstriction followed by vasodilatation.
 The vasoconstriction may be due to a response triggered
by the trigeminal nerve, which stimulates release of
substance P, a pain transmitter, into the vessels or by the
release of amines such as serotonin, norepinephrine, and
epinephrine.
24/10/2023
265
A migraine may or may not begin with an aura (visual

phenomena, such as a flashing light that precedes an
attack
Commonly used descriptors of migraine pain include
throbbing, boring and pounding
It is usually on one side of the head(unilateral )
Noise and light tend to exacerbate the headache
 leading the patient to rest in a dark, quiet environment.
24/10/2023
266
 the cause of migraine is often unknown, common precipitants

 Family history of migraine present in nearly 2/3 of patients.
 Environmental, dietary and psychological factors.
 Emotional stress , depression
 Altered sleep pattern
 Oral contraceptives
 menstrual cycle
 Alcohol intake especially red wine
 Caffeine withdrawal
 Various food staffs ( e.g. chocolates, cheese , meals containing
nitrates
24/10/2023
267
There are two types of migraine headaches:

 classic migraine and common migraine.
 The classic migraine has a preheadache (prodromal)
phase in which the patient may experience
visual disturbances, difficulty with speaking, and/or
numbness or tingling, depression ,restlessness, irritable
24/10/2023
268
The headache that follows is often accompanied by

nausea and sometimes vomiting, and may last for hours to
days.
 A common migraine does not have the preheadache
phase, but the patient experiences an immediate onset of a
throbbing headache
24/10/2023
269
 Prophylactic Treatment: includes drug regimens and changes in

patients behavior
 Prophylactic treatment is indicated if the patient has three or more
attacks per month.
 Drugs used for this purpose include β-blockers (propranolol),
Calcium channel blockers (Verapamil ,Tricyclic antidepressants
(amitriptyline)
 Dietary restrictions may be helpful if precipitating foods or
beverages can be identified.
 Biofeedback therapy
 It is simple and cost effective. by helping patients deal more
effectively with stress
24/10/2023
270
 Acute attack
 NSAIDS (Nonsteroidal antinflamatory agents): such as
ASA, paracetamol, Ibuprofen, Diclofenac
 Reduce the severity and duration of migraine attack. for
mild to moderate attacks
 Are most effective when taken early.
 Ergot preparations: Ergotamine and dihydro-ergotamine)
Can be given oral, sublingual, rectal, nasal and parentral
preparation.
 Dose: 1 – 2 mg oral
24/10/2023
271
Cluster Headaches
Vascular disturbance, stress, anxiety, and emotional
distress are all proposed causes of cluster headaches.
As indicated by the name, these headaches tend to occur
in clusters during a time span of several days to weeks.
 Alcohol consumption may worsen the episodes.
The patient may state that the headache begins suddenly,
typically at the same time of night. Throbbing and
excruciating pain .
24/10/2023
272
The headache tends to be unilateral, affecting the nose, eye,

and forehead. A bloodshot, teary appearance of the affected
eye is common, nasal stiffness
During attack patients often have associated nasal stiffness,
lacrimation and redness of the eye ipsilateral to the
headache.
Alcohol provokes attacks in about 70% of patients
Because of the brief nature of cluster headaches, treatment
is difficult.
A quiet, dark environment and cold compresses may
decrease the intensity of the pain.
24/10/2023
273
 Treatment
 Acute attack (Treatment)
 NSAID
 Inhalation of 100% oxygen and
 ergotamine .
 Sumatriptan
 Preventions/prophylactic therapy:
 Prednisolone , Lithium, Methysergide, Ergotamine,
Sodium valproate and verapamil
24/10/2023
References
274
 Suzanne C. O’Connell Smeltzer, & Brenda G. Bare. (2004).

Brunner and Suddarth’s Text Book of Medical-Surgical
Nursing. 10th Edition.
 Lewis,M.S.,Heitkemper,M.M.,and Dirksen,.R..S.
(2000).Medical Surgical Nursing :Assessment And
Management Of Clinical Problems .5th Ed.
 Kasper L, Braunwald E.(2005). Harrison’s princeples of internal
medicine,16th Edition.
 Porth C.(1989). Pathopysiology concepts of alterd health states. 4th
Ed
 Myers R.Allen,(2003) .National medical series for independent study
(NMS)3 th Edition.
24/10/2023
References
275
 Barbara B.(1995) A Guide to physical examination

and history taking,6 th Edition.
 http://www.medicinenet.com/seizure.
 Teklehaymanot R (1986) prevalence of active
epilepsy in Addis Ababa.
 Beare,G.P. &Myers,J.(1990).Principles And
Practice Of Adult Health Nursing.
24/10/2023
276
Thank
you!
24/10/2023276

Neurological Disorders For BSC

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1

 Describe the causes, pathophysiology, clinical

 Head injury, Spinal cord injury

 Bell’s palsy(Facial paralysis)

 Parkinson’s diseases, Headache(cephalgia)

Cells of the Nervous System

Intra cranial pressure(ICP)

 The pressure is measured via the CSF, the normal

The rigid cranial vault contains brain tissue

 ICP will begin to rise under normal

Common causes of increased ICP

 Increased ICP due to increased CSF volume,

 change LOC (Early sign )

 Double vision (diplopia)

Vital sign changes are a late indication of Increased

 Detecting Later Signs of Increased ICP

 History and physical examination

DECREASING CEREBRAL EDEMA

3,Other method for decreasing cerebral

dehydration and hemoconcentration

 Elevating the patient’s head to optimize venous

4.Preventing a Temperature elevation (because fever

6.MAINTAINING CEREBRAL PERFUSION

7 MAINTAINING A PATENT AIRWAY

 Proper positioning helps to reduce ICP,The head is

 Stool softeners may be prescribed.

1, Brain herniation(is a shifting of brain contents from a

 Resulting from sudden excessive discharge from

Classification of seizures based on the international

Partial Generalized Unclassified

Seizures beginning Involve electrical i. Neonatal seizures

2.Generalized Seizures (convulsive or

i. Absence seizures ( petit mal )

ii. Tonic – clonic seizures ( grand mal )

iii. Myoclonic seizures

iv. Clonic seizures

vi. Atonic seizures

Etiology of seizure or risk factors:

1. Partial Seizures (focal seizures)

B. Complex partial seizure

B. Complex partial seizure

PARTIAL SEIZURES. Repetitive, purposeless behaviors,

Patients may be labeled as mentally ill, particularly if

loss of postural control.

 It is usually detected by unexplained daydreaming and

ii. Generalized tonic clonic seizure(Grand mal)

 After 10 – 20sec tonic phase evolves to clonic phase

iii. Myoclonic seizure

 Sudden and brief muscle contraction

 Involve one part of the body or the entire.

iv. Atonic Seizures

 DX is aimed at the types of seizure, their

Epilepsy is estimated to affect 0.5-4% of the population

In Ethiopia, based on a study done by

It is estimated that 5-10% the population will

It is estimated that 5-10% the population will have at

is a group of syndromes characterized by recurring

Messages from the body are carried by the neurons

 Idiopathic or cryptogenic ;in which the cause is

 head injuries, brain tumors ,abscess, and congenital

 Treatment of underlying condition

 Avoidance of precipitating factor