NURSING INTERVENTION OF PATIENTS

WITH NEUROLOGIC DISORDERS

By:- Girma.Y
Dec. 28/11/2024

1
 At the end of this chapter, students will be able to describe:
 Describe anatomy and physiology review of nervous
system
 Explain how to take history and physical examination
of patient with neurologic problem
 Discuss the common diagnostic techniques and nursing
responsibilities of neurological disorders
 Discuss neurologic system disorders in terms of
(descriptions, risk factor/etiology, pathophysiology,
classifications, clinical manifestation, assessment and
diagnosis, management (medical, surgical and/or nursing
using nursing process) and prevention,2 complications)
 Introductio  Autoimmune
–n Anatomy & physiology disorders
review  Cranial nerve
– History & Physical disorders
examination
– Diagnostic techniques  Peripheral nervous
 Headache system disorder
 Cerebrovascular accident  Traumatic lesions
 Brain tumor  Degenerative
 Brain Abscess disorders
 Seizure & Epilepsy
 Infectious neurological
problems 3
 Increased intracranial  Meningitis
pressure  Encephalitis
 Seizure
 Poliomyelitis
 Epilepsy
 Myasthenia
 Headache Gravis
 Ischemic stroke  Bell’s palsy
 Hemorrhagic stroke  Neuropathy
 Head injury  Parkinsonism
 Brain injury
 Spinal cord trauma

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 Brain storming
Be in group and discuss the following
 What is NS?
 What are the major classification of NS
 What are Cells of NS & their function
 Function of NS?
 How NS can be assessed?
 List equipment used during NS examination

01/04/2025 Neurologic Disorders 5

 The nervous system consists of two
major parts:
– The central nervous system (CNS), Fact:
**Brain contains
including
1. The brain &Spinal more than 100 billion
cord, cells
– The peripheral nervous system, **Links motor &
which includes: sensory
1. The cranial nerves,  monitor the
body’s
2. Spinal nerves, and processes,
 respond to the
3. Autonomic nervous
internal &
system. external
 The function of the nervous system environment,
is:  Maintain
homeostasis,
– To control motor, sensory, autonomic,  direct all
cognitive, & behavioral activities. psychological,
6 biologic, &
 Cells of the Nervous
System
 The basic functional unit of the brain is
the neuron 2. Axon: Long projection that
carries
electrical impulses away from the cell
body.

1.
Dendritis:
branch-type
structures
for receiving  A cluster of cell
electrochemi bodies
cal with the same function
messages 3. Nerve cell bodies: is called center
occurring in clusters are
 Cells of the Nervous
System...
 Neuroglia( glial cells) it provide support, nourishment, and
protection to neurons.
– They constitute almost half the brain and spinal cord mass
and are 5 to 10 times more numerous than neurons
– Most of brain tumors rises from Glia cells(45%)
Types of glial cells.
1. Oligodendrocytes are specialized cells that produce the
myelin sheath of nerve fibers in the CNS
2. Astrocytes provide structural support to neurons, and
their delicate processes form the blood-brain barrier.
3. Ependymal cells line the brain ventricles and aid in
the secretion of cerebrospinal fluid (CSF).

4. Microglia, a type of macrophage, are relatively rare

in normal CNS tissue. They are phagocytes and are
t
important in host defense y
 Neurotransmitte
rs
 Manufactured and stored in synaptic
vesicles
 Communicate messages from:
– one neuron to another, or
– from a neuron to a target cell
 Transported across the synapse,
 Binding to receptors on the postsynaptic cell
membrane
 Either excite or inhibit activity of the target
Note: All brain functions are modulated through neurotransmitter
cell.
receptor site activity, including memory and other cognitive processes
9
 Major
Neurotransmitters

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 The Central Nervous System
 The brain accounts for ~ 2% of the total
body weight
An average young adult, ~1400 g
In average older adult~1200 g
The brain is divided
into three major areas:
1. the cerebrum,
2. the brain stem, &
3. the cerebe lum
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 The cerebrum is composed of:
1. Two hemispheres,
2. The thalamus,
3. The hypothalamus, &
4. The basal ganglia.
 The brain stem includes:
1. The midbrain,
2. Pons, &
3. Medulla
 The cerebellum is located under the cerebrum & behind
the brain stem.

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Cerebrum
 Cerebral hemispheres is separated by the great longitudinal
fissure into the right and left hemispheres.
 The two hemispheres are joined at the lower portion of the fissure
by the corpus callosum
 Outer portion of the hemispheres is made up of gray matter(2-
5mm depth) & it contains billions of neuron cell bodies
 White matter (innermost layer) & is composed of myelinated
nerve fibers & neuroglia cells forms pathways connecting various
parts of the brain with one another
 These pathways also connect the cortex with lower portions of the
brain & spinal cord.
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 The cerebral hemispheres are divided into pairs of lobes
as follows:
1. Frontal—the largest lobe, located in the front of the
brain.
– concentration, abstract thought, information storage or
memory, and motor function.
– Contains Broca area, located in the left
hemisphere
 is critical for motor control of speech.
– Also responsible in large part for a person’s affect,
judgment, personality, and
inhibitions
2. Parietal—a predominantly sensory lobe posterior to
the frontal lobe.
– Essential to a person’s awareness of body position in
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space, size and shape
3. Temporal—located inferior to the frontal and parietal
lobes,

– contains the auditory receptive areas &

– plays a role in memory of sound & understanding of

language and music.

4. Occipital—located posterior to the parietal lobe,

– responsible for visual interpretation and memory.

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 The corpus callosum, a
thick collection of nerve
fibers that connects the
two hemispheres of the
brain,
 responsible for the
transmission of information from
one side of the brain to the
other.
 Information transferred
includes sensation,
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The thalamus act primarily as a relay station for all sensation
except smell
– All memory, sensation, and pain impulses pass through this
section of the brain.
The hypothalamus
– regulates the pituitary secretion of hormones of endocrine
system
– Works with the pituitary to maintain fluid balance through
hormonal release and maintains temperature regulation by
promoting vasoconstriction or vasodilatation.
– is the site of the hunger center and is involved in
appetite control.
– Contains centers that regulate the sleep–wake cycle, blood pressure,
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 The basal ganglia are masses of nuclei located deep
in the cerebral hemispheres
– responsible for control of fine motor movements, including those
of the hands & lower extremities.

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 The brain stem consists of the midbrain, pons, and
medulla oblongata

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 The midbrain -connects the pons and the cerebellum
with the cerebral hemispheres;
– it contains sensory and motor pathways & serves as the center for
auditory & visual reflexes.
– Cranial nerves III and IV originate in the midbrain.
 The pons is situated in front of the cerebellum between the
midbrain and the medulla
– Cranial nerves V through VIII originate in the pons.
– The pons also contains motor and sensory pathways.
– Portions of the pons help regulate respiration

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The medulla:
 Motor fibers from the brain to the spinal cord and sensory
fibers from the spinal cord to the brain are located in the
medulla.
 Most of these fibers cross, or decussate, at this
level.
 Cranial nerves IX through XII originate in the medulla.
 Reflex centers for respiration, blood pressure, heart
rate, coughing, vomiting, swallowing, and sneezing are
also located in the medulla.
 The reticular formation, responsible for arousal and the
sleep–wake cycle, begins in the medulla
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and connects with
 The cerebellum is posterior to the midbrain and pons,
and below the occipital lobe
 The cerebellum integrates sensory
information to provide smooth coordinated
movement.
 It controls fine movement, balance, and
position (postural) sense or proprioception
(awareness of position of extremities without
looking at them).

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 Skull
– The brain is contained in the rigid skull, which protects it
from injury.
– The major bones of the skull are the frontal,
temporal, parietal, occipital, and sphenoid
bones.
– These bones join at the suture lines and form the
base of the skull.
Indentations in the skull base are known as fossae.
 The meninges
It covers the brain & spinal cord
provide protection, support, and nourishment to the
brain and spinal cord.
The layers of the meninges are
 the Dura, Arachnoid, & Pia mater.
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 Cerebrospinal fluid(CSF):

– 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. 25
 The cerebral circulation receives15% of the cardiac
output, or 750 mL per minute.
 Two internal carotid arteries and two vertebral arteries
provide the blood supply to the brain.
 The brain does not store nutrients
– requires a constant supply of oxygen and glucose.
– uses 20% of the body's oxygen and 25% of its glucose
– blood pathway is unique because it flows against
gravity;
– Its arteries fill from below and the veins drain from
above
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 At the base of the brain surrounding the pituitary
gland, a ring of arteries is formed between the
vertebral and internal carotid arterial chains.
– This ring is called the circle of Willis

– formed from the branches of the internal carotid arteries,

anterior and middle cerebral arteries, and anterior and

posterior communicating arteries
 It provide collateral circulation if one or more of
the four vessels supplying it become occluded
or are ligated.
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 Normal Cerebral Perfusion Pressure (CPP) is 70 to
100 mm Hg.
 CPP < 50 mm Hg is associated with ischemia and
neuronal death
 CPP = MAP − ICP
 Example: Systemic blood pressure = 122/84
– MAP = 97 ,ICP = 12 mm Hg, CPP = 85 mm Hg
 CPP, Cerebral perfusion pressure;
 DBP, diastolic blood pressure;
 ICP, intracranial pressure;
 MAP, mean arterial pressure;
 SBP, systolic blood pressure

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 Neurologic diseases are common and costly.
 According to estimates by the World Health
Organization:
– neurologic disorders affect more than 1 billion people worldwide,
– constitute 12% of the global burden of disease, and
– cause 14% of global deaths
 skillful approach to diagnosis is essential
 begins with the patient and focuses the clinical problem first
in anatomic & then in pathophysiologic terms
 Once the question, “Where is the lesion?” is answered,
then the question
“What is the lesion?” can be addressed
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 An important aspect of the neurologic
assessment is the history of the present
illness.
 The health history therefore includes details
about:
– the onset, character, severity, location, duration, and
frequency of symptoms and signs;
– associated complaints; precipitating, aggravating, and
relieving factors;
– progression, remission, and exacerbation; and
– the presence or absence of similar symptoms
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among family
Common Symptoms
 Pain
 Seizures
 Dizziness and Vertigo
 Visual Disturbances
 Muscle Weakness
 Abnormal Sensation

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 Common Symptoms
Pai
n
 In neurological disease an acute pain may be associated
with
– brain hemorrhage,
– spinal disc disease or
– trigeminal neuralgia.

 In contrast, chronic or persistent pain extends for long

periods of time and may represent a broader
pathology.
– can occur with many degenerative33and chronic neurologic
 Common Symptoms
Seizures
 Result of abnormal electrical discharges in the cerebral
cortex,
 Manifest as an alteration in sensation, behavior,
movement, perception, or consciousness
– May be short, as in a blank stare that lasts only a second, or
– Longer duration, such as a tonic–clonic grand mal seizure _last
several minutes.
 Reflects the area of the brain affected.
 Can occur as isolated events, _induced by a high fever,
alcohol or drug withdrawal, or hypoglycemia.
 A seizure may also be the first obvious
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sign of a brain
 Past Health, Family, and Social History
 Any family history of genetic diseases
 A review of the medical history,
 History of trauma/falls that may have involved the
head/spinal cord.
 The use of alcohol, medications, and illicit drugs
are also relevant.
 The history-taking portion of the neurologic assessment is
critical &, in many cases of neurologic disease, leads to an
accurate diagnosis.
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 The brain and spinal cord cannot be examined as
directly as other systems of the body.
 Much of the neurologic examination is an indirect
evaluation that assesses the function of the specific
body part or parts controlled or innervated by the
nervous system.
 A neurologic assessment is divided into five
components:
 cerebral function, cranial nerves, motor system, sensory
system, and reflexes

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 Assessing Cerebral Function
 Mental status
– An assessment of mental status begins by
observing the patient’s appearance and behavior,
noting dress, grooming, and personal hygiene.
– Posture, gestures, movements, facial expressions.
– The patient’s manner of speech and level of
consciousness
– Assessing orientation to time, place, and person .

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38
 Examining the Cranial Nerves

 Cranial nerves are assessed when:

– level of consciousness is decreased,

– with brain stem pathology, or

– in the presence of peripheral nervous system

disease

 Right and left cranial nerve functions are compared

throughout the examination.

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General inspection
 Perform a brief general inspection of the patient, looking
for clinical signs suggestive of underlying pathology:
 Speech abnormalities: may indicate glossopharyngeal or
vagus nerve pathology.
 Facial asymmetry: suggestive of facial nerve palsy.
 Eyelid abnormalities: ptosis may indicate oculomotor
nerve pathology.
 Pupillary abnormalities: mydriasis occurs in oculomotor
nerve palsy.
 Strabismus: may indicate oculomotor, trochlear or
abducens nerve palsy.
 Limbs: pay attention to the patient’s arms and legs as they
enter the room and take a seat noting any
40 abnormalities (e.g.
 To test cranial nerve I..
….olfactory nerve

CN II-Optic nerve
Confrontation Visual
Field Test
V
i
s
u
a
l
a
c
u
i
t 41
y
Cranial Nerve III, IV,
VI

By 42
Abdulwahid A
 To test Cranial Nerve V…..trigeminal nerve
• Have the patient bite down and feel the masseter muscle and
temporal muscle
• Then have the patient try to open the mouth against resistance

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 To test cranial nerve VII…facial nerve:
– have the patient close their eyes tightly, smile, frown,
puff out cheek.
– Can they do this will ease?

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 Cranial Nerve VIII  vestibulocochlear nerve:
– Test the hearing by occluding one ear and whispering
two words and have the patient repeat them back.
– Repeat this for the other ear.
 Cranial Nerve I X (glossopharyngeal) and X
(vagus)
– have patient say “ah”…the uvula will move up (cranial
nerve IX
intact)
– if the patient can swallow with ease & has no
hoarseness when talking, cranial nerve
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X is
 Cranial Nerve X I (accessory nerve)
– Have the patient move head from side to side and up
and down and shrug shoulders against resistance.

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 Cranial Nerve X I I (hypoglossal)
– have patient stick tongue out and move it
side to side

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 Examining the Motor System

 includes: an
assessment of

– Muscle size and tone

– Muscle strength

– Balance and
coordination

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 The muscles are inspected, and palpated
– for their size and symmetry.
– Any evidence of atrophy or involuntary movements
(tremors, tics)
 Muscle tone (the tension present in a muscle at rest) is
evaluated by palpating various muscle groups at rest
and during passive movement.
 Resistance to these movements is assessed and
documented.
 Abnormalities in tone include:
– spasticity (increased muscle tone),
– rigidity (resistance to passive stretch),
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and flaccidity
 The five-point scale is used to rate and record distal
and proximal
strength in both upper and lower extremities

1. A 5 indicates full power of contraction against

gravity and resistance or normal muscle strength;
2. 4 indicates fair but not full strength against gravity
and a moderate amount of resistance or slight
weakness;
3. 3 indicates just sufficient strength to overcome the
force of gravity
or moderate weakness;
4. 2 indicates the ability to move but not to overcome the
force of gravity or severe weakness;
5. 1 indicates minimal contractile power (weak muscle
contraction can be palpated but no movement is noted) or
very severe weakness; and 50
6. 0 indicates no movement
Balance & Coordination
 Cerebellar & basal ganglia  pat their thigh as fast as possible
influence on the motor with each hand separately.
 pronate and supinate the hand
system is reflected in as rapidly as possible.
balance control and  touch each of the fingers with the
thumb in a consecutive motion.
coordination.  Speed, symmetry, and degree
 Coordination in the hands & of difficulty are noted.
 Point-to-point testing is accomplished
upper extremities is tested by having the patient touch the
by having the patient examiner’s extended finger and then
their own nose.
perform  This is repeated several times.
– rapid,
alternating
movements & 51
 Point-to-point testing

rapid, alternating
movements
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 Coordination in the lower extremities is tested by:
– having the patient run the heel down the anterior surface of the tibia of
the other leg.
– Each leg is tested in turn.
– Ataxia is an incoordination of voluntary muscle action, particularly
of the muscle groups used in activities such as walking or reaching
for objects.
 Tremors (rhythmic, involuntary movements) noted at rest or
during movement
suggest a problem in the anatomic areas responsible for balance and
coordination.
run the heel
down
 Gait
 Gait is evaluated by having the
patient walk across the room
under observation.
 Gross gait abnormalities should be
noted
 Next ask
– the patient to walk heel to toe
across the room,
– then on their toes only, and
finally on their heels only.
– Normally, these maneuvers
possible without too much
difficulty.
 Also, hopping in place on
each foot 54
 The Romberg test is a screening test for balance
– can be done with the patient seated or standing.
– The patient can be seated or stand with feet together and arms
at the side,
– test first, with eyes open and then with both eyes closed for 20
seconds

55
Examining sensory system
 Assessment of the sensory system involves:
– light touch sensation (brush) &pain sensation (pin
prick),

 Stereognosia vs. Astereognosis

or tactile agnosia
–lesion in the
sensory cortex of the
parietal lobe.
 position sense
(proprioception).

G
By r 5 l of Nursing © 2022, Jimma
University
Abdulwahid
 Agnosia is the general loss of ability to recognize objects through
a particular sensory system. Each of these dysfunctions implicates
a different part of the brain

57
 Examining the Reflexes
 Reflexes are involuntary contractions of muscles or
muscle groups in response to a stimulus.
 Reflexes are classified as
– deep tendon,
– superficial, or
– pathologic

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 Documenting Reflexes
Deep tendon reflexes are graded on a scale of
0–4:
 0 No response
 1+ Diminished (hypoactive)
 2+ Normal
 3+ Increased (may be interpreted as normal)
 4+ Hyperactive (hyperreflexia)

 The deep tendon responses & plantar reflexes are commonly

recorded on stick figures.
 The arrow points downward if the plantar response is normal and
upward if the response is abnormal.

t
y
Major reflexes
A. Eliciting the biceps reflex.
B. Eliciting the triceps reflex.
C. Eliciting the patellar reflex.
D. Eliciting the Achilles

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 CT scan, MRI
 Electroencephalogram (EEG)
 Electrodiagnostic tests, such as electromyography (EMG) and
nerve conduction velocity (NCV)
 Positron emission tomography (PET)- measures the metabolic
activity of cells.
 Arteriogram (angiogram). detects blockage or narrowing of the
vessels.
 Cerebrospinal Fluid Analysis
 Evoked potentials,
 Myelogram
 Neurosonography
 Ultrasound (sonography) 61
 1. Increased intracranial
pressure
2.Seizure disorders
 The epilepsies
 Status epilepticus

1.Headache

62
 6
2

INCREASED INTRA-CRANIAL PRESSURE(IICP)

Intra cranial pressure(ICP)
 is the pressure exerted in the cranium by its
contents:
 The brain tissue ,Blood, and
cerebrospinal fluid(CSF)
The pressure is measured via the CSF, the

normal pressure of CSF IS 5-15mmHg or 60-

180mmH2O,
pressure over 250mmH2O is called increased ICP,
 Is a symptom of serious underlying
64
disorder.
 The rigid cranial vault contains
1. brain tissue (1,400 g),
2. blood(75 mL), and
3. CSF (75 mL)

 The volume and pressure of these three

components are usually in a state of equilibrium
and produce the ICP.

65
 The modified Monro-Kellie doctrine describes
– the relatively constant volume of these three
components within the rigid skull structure.
 If the volume of any one of the three
components increases within the cranial vault
and the volume from another component is
displaced, the total intracranial volume will not
change.
 This hypothesis is only applicable in
situations in which the skull is rigid (e.g., the
hypothesis is not valid in neonates & in adults with
66
 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
67
 ICP will begin to rise under normal circumstances
in the following conditions

– Minor changes in blood volume & CSF volume occur

constantly due to alterations in intrathoracic pressure.

– coughing, sneezing, straining, posture, blood pressure, and systemic

oxygen and carbon dioxide levels.

68
 Increased Intracranial Pressure
cont
68

Pathophysiology
Increased ICP is a syndrome that affects many patients
with acute neurologic conditions.
This is because pathologic conditions alter the
relationship between intracranial volume and pressure.
 69

 Most commonly associated with head injury,

 it also may be seen as a secondary effect in other conditions, such

as
 braintumors, subarachnoid hemorrhage, and toxic and viral
encephalopathies
 Increased ICP from any cause:

 decreases cerebral perfusion,

 stimulates further swelling (edema), and
 shifts brain tissue through openings in the rigid dura,
resulting in herniation, a dire, frequently fatal event.
 70

Pressure Changes.
The relationship of pressure to volume is depicted in the
pressure- volume curve.
Compliance is the expandability of the brain.
It is represented as the volume increase for each unit
increase in pressure. With low compliance, small
changes in volume result in greater increases in
pressure.
 Compliance = Volume / Pressure
 74

Common causes of increased ICP

 Head trauma(injury )
 Intracranial hemorrhage,

 Hematoma, cerebral edema

 Brain tumors (increasing tissue volume)

 CNS infection eg: meningitis,Toxoplasmosis,

cryptococal meningitis ,cerebral malaria

 Brain abscess
 Increased Intracranial Pressure
cont
75

Increased ICP due to increased CSF

volume can result from
 increased CSF production,
 impaired reabsorption ,
 blocked flow
 Hydrocephalus
 Increased Intracranial Pressure
cont
76

 DECREASED CEREBRAL BLOOD FLOW

 Increased ICP may significantly reduce cerebral blood
flow,
resulting in ischemia and cell death.
 In the early stages of cerebral ischemia, the vasomotor

centers are stimulated and the systemic pressure rises

to maintain cerebral blood flow.

Usually a slow bounding pulse and respiratory
irregularities accompany this.
 Increased Intracranial Pressure
cont
77

 These changes in blood pressure, pulse, and

respiration are important clinically because they

suggest increased ICP.
Increased ICP caused by increased blood volume

results from Vasodilatation

The [CO2] in the blood and in the brain tissue also

has a role in the regulation of cerebral blood flow.

A rise PaCO2 causes cerebral vasodilatation,
 Increased Intracranial Pressure cont
78

Increased PaCO2 is leading to increased

cerebral blood flow and increased ICP;
 a fall in PaCO2 has a vasoconstrictive effect.

Decreased venous outflow may also increase

cerebral blood volume, thus raising ICP
 Increased Intracranial Pressure cont
7
9

 CEREBRAL E D E M A

 Cerebral edema or swelling is defined as an

abnormal accumulation of water or fluid in the

intracellular space, extracellular space, or both,
associated with an increase in brain tissue
volume
 Increased Intracranial Pressure cont
8
0
Edema can occur in the gray, white, or interstitial
matter.
As brain tissue swells within the rigid skull, several
mechanisms attempt to compensate for the IICP.
These mechanisms include auto-regulation and
decreasing the production and flow of CSF.

Auto-regulation refers to the brain’s ability to

change the diameter of its blood vessels
automatically to maintain a constant cerebral blood
flow during alterations in systemic blood
pressure
 Increased Intracranial Pressure cont
81

CEREBRAL R E S P O N S E T O I N C R E A S E D
ICP
 As ICP rises, compensatory mechanisms in the

brain work to maintain blood flow and prevent

tissue damage.
 The brain can maintain a steady

perfusion pressure when the arterial

systolic blood pressure is 50 to 150 m m
H g and ICP is less than 40 mmHg.
 Increased Intracranial Pressure
cont
82

 The cerebral perfusion pressure (CPP) is

calculated by subtracting the ICP from MAP

For e.g.
 If the MAP is 100 and the ICP
is 15,
 Then the CPP is 85 mm Hg.

 The normal CPP is 70 to

100 mm Hg
 Increased Intracranial Pressure cont
83

As ICP rises, however, and the autoregulatory

mechanism of the brain is overwhelmed,

 CPP can rise to >100 mm Hg or fall to <50 mm Hg.

Patients with a CPP less than 50 mmHg

experience irreversible neurologic

damage.
 If ICP = MAP ,cerebral circulation
ceases
 Clinical Manifestations
84
 Change LOC (early sign )
 Restlessness, confusion, or
 Increasing drowsiness
 Headache that is constant, increasing in
intensity, and aggravated by movement or
straining.
 Vomiting , papillae edema
 Double vision (diplopia)
 Clinical Manifestations
85

 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 a clinical

phenomenon known as the Cushing’s response (or

Cushing’s reflex) is seen when cerebral blood flow
decreases significantly.
 When ischemic, the vasomotor center triggers a rise in

arterial pressure in an effort to overcome the increased

ICP.
 Clinical Manifestations
86

Cushing’s triad includes:

1. A rise in systolic blood pressure,(arterial
hypertension)

2. Slowing of the heart rate(bradycardia),

3. Bradypnea,
 This is a sign requiring immediate
intervention; however,
perfusion may be recoverable if treated rapidly.
 Clinical Manifestations cont’d
87
 Detecting Later Signs of Increased ICP
 LOC continues to deteriorate until the patient is comatose.
 Cheyne-Stokes breathing

 Projectile vomiting may occur with increased pressure

on the reflex center in the medulla.

 As neurologic function deteriorates further,
– becomes comatose and exhibits abnormal motor

responses in the form of decortication, decerebration,

or flaccidity.
– then, the pupils dilated & fixed and respirations impaired,

death is usually inevitable.

 Hemiplegia (when pressure on the brain stem
increases)
 Diagnostic Findings
88

 History and physical examination

 Computed tomography (CT)scanning
 Magnetic resonance imaging (MRI)
 Cangiography
 Skull x ray

NB: Lumbar puncture is avoided in patients with increased ICP because

the sudden release of pressure can cause the brain to herniation
 Management
89

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.
 90

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
 91

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. M A I N TA I N I N G OX Y G E N AT I O N
 Arterial blood gases must be monitored to ensure that
systemic oxygenation remains optimal
 Hyperventilation is recommended
 92

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 .
 93

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
 94

 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
 95

 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.
 96

Surgical Management
Reducing CSF and intracranial

blood volume CSF drainage is

frequently performed by:

 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
97
 98

 Brain stem herniation

– results from an excessive increase in ICP, when the

pressure builds in the cranial vault and
☑the brain tissue presses down on the brain stem.

– This increasing pressure on the brain stem results in

the cessation of blood flow to the brain,
☑causing irreversible brain anoxia and brain death.
 99

 Diabetes insipidus

– is the result of decreased secretion of antidiuretic hormone.

– The patient has excessive urine output, and hyperosmolarity
results.

 SIADH

– SIADH is the result of increased secretion of antidiuretic

hormone.
– The patient becomes volume-overloaded, urine output
diminishes, and serum sodium concentration becomes dilute.
 10
0

Seizure & Epilepsy

 Learning objectives
10
1

⚫ Define Seizure & epilepsy

⚫ Describe the international classification of Seizure.

⚫ List the etiologies or risk factors for Seizure disorder

⚫ To identify the clinical manifestation of different types

of Seizure disorders
⚫ To understand the diagnostic approaches & patient
management
⚫ To aware the complication of seizure/epilepsy: status
epilepticus
 Seizure Disorders
10
2

 Episodes of
abnormal:
 Motor
 Sensory
or a
 Autonomic combination
 Psychic
activity
 that result from sudden excessive discharge from
cerebral neurons.
 A part or all of the brain may be involved.
 Seizure…
 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:

– either a symptom of epilepsy or

– other neurological disorders such as a brain tumor or
meningitis.
 Seizure…
Classification of seizures based on the
international Seizure classification society.
SEIZURE

Partial Generalized Unclassified

Involve electrical
Seizures beginning discharges in the
Locally(focal seizure)whole brain
 Seizure- Classification
 Partial Seizures (focal  Generalized
seizures) seizures
1. Simple partial seizure
1. Absence seizures ( petit mal
• known as Jacksonian & focal )

motor 2. Tonic – clonic seizures

2. Complex partial ( grand mal )
seizure
3. Myoclonic seizures
1. psychomotor
seizures,Temporal
4. Clonic seizures
lobe seizures
5. Tonic Seizures
Seizure
…
 Seizure- Etiology of seizure or risk factors:
 Idiopathic or cryptogenic (70%)
 Genetic factor (Family History) ,  Metabolic and toxic condition

 Developmental defects (Hypoglycemia,Hypocalcemia,Hypon

 at ermia,Renal failure,Pesticides)
Acquired hypoxemia of any
 Head trauma, Neoplasms, after brain
causes, Fever (child hood),Vascular
surgery
insufficiency, Hypertension, stroke
 Allergies, Drugs,Alcohol & others
 CNS infections
(toxoplasmosis, meningitis ,
 Seizure-Clinical features
A. Simple Partial B. Complex partial
Seizures: seizure:
 Consciousness is not
 Impaired
impaired  Unable to respond
 Motor, sensory, autonomic or consciousness
psychiatric. appropriately to visual or
 Angle of mouth may jerky verbal commands
 Only Finger or hand may during the seizure.
shake  Begins with an
 Person may experience aura(warning sign)
unusual or unpleasant  Start of the ictal phase
sights, sounds, odors or is often a sudden
tastes behavioral arrest or
 Seizure- C/features…
Complex partial seizure…
 Repetitive, purposeless behaviors, called automatisms,

are the classic symptom of partial seizures,

 the patient is not aware of the behavior may
occur
– Chewing
– lip smacking
– Patting
– picking movement of the hands, picking at cloths
– Staring
– display of emotions.
 Seizure- C/features…
Note:
⚫ 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 ,Amnesia and transition
to full recovery may take minutes to hours.
 Generalized Seizure- C/M
Absence seizure
(petit-mal)
Common in children
 Sudden & 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.
 The patient returns to base line immediately
after the seizure
 Generalized seizure C/M ……
 There is no post-ictal confusion.
 It is usually detected by unexplained daydreaming &
decline in school performance.
 usually begins in childhood (4-8 yrs), & has a good
prognosis,
 60-70% of such patients have spontaneous
remission during adolescence.
 Generalized Seizure- C/feature
Generalized tonic clonic seizure(Grand mal)
 The most common seizure type(60%)
 Ictal phase –
 tonic contraction of muscles throughout the body
 immediate loss of consciousness

 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
 Generalized Seizure- C/feature
Generalized tonic-clonic
seizure
 After 10 – 20sec tonic phase evolves  clonic phase

 Clonic phase lasts for another 1 minute

 bilateral jerking clonic movement involving the whole

body.
 Contraction with relaxation of major muscles
 The patient is incontinent of urine and stoo
 Biting the lips or tongue may cause bleedin
 Generalized Seizure- C/feature
Myoclonic seizure
Atonic Seizures
 Sudden and brief
 Sudden loss of
muscle
contraction
postural muscle tone,

 Involve one part of the lasting 1 to 2

body or the entire Seconds.
 Can be physiologic or  Consciousness is
pathologic.
briefly impaired
 Is most commonly seen
 Usually manifest as a
with metabolic disorders,
degenerative diseases of head drop or nodding
the CNS or anoxic brain movement
 Seizure- Ass’t & Dx
Diagnosis is aimed at the types of seizure, their
frequency & 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
 Seizure- Ass’t & D x …
 EEG (Electroencephalography)

 A graphic recording of  Other routine laboratory

the electrical activity of assessment
the superficial layers of  CBC.
the cerebral cortex.  Urinalysis
 Aids in classifying the  Serum
types of seizure and the glucose(FBS,RBS)
treatment  Liver function test
 RFT
 Neuroimaging preferably
 Electrolytes
MRI,CT scan
test
 Epilepsy
 Epilepsy - 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
Secondar
Primary y
Idiopathic Symptom of
another underlying
condition.
 Epilepsy
Note:
 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.
 Epilepsy- Pathophysiology
 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
Epilepsy- Etiology

2
 Epilepsy-Management
122

 Treatment of underlying condition

 Avoidance of precipitating factors:

 increased physical activity ,emotional stress, excessive
fatigue ,alcohol, caffeine ,certain foods or chemicals

 Suppression or control of recurrent seizure

 Antiepileptic drug therapy (AEDT)

 Epilepsy-Management…
Pharmacologic therapy
 The objective is to achieve seizure control with minimal side
effects.
 Medication therapy controls rather than cures
seizures.
 Selected on the basis of the type of seizure being

treated & the effectiveness & safety of the

medications .
⚫ 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
 Epilepsy-Management…
Phenobarbitone
 is the drug of choice for the
Phenytoin
• Usual prescribed as a 2nd
control of partial and GTC
line drug in resource limited
seizures, in developing countries
settings.
 Dosage forms: 15, 30, 60
• Dosage: 100 mg PO BID or
&100 mg tabs. TID
 Starting dose-60mg(Adut) • gradually increased to a
PO daily. max of 200 mg PO TID.

 If seizure is not controlled the

• Side effects:
dosage may be increased gradually. • Gingival hyperplasia
• Coarsening of facial
 If Rx fails or poor control with
• feature
maximum • Toxic hepatitis
, tolerable doses, a 2nd AEDS is
often added.
 Epilepsy-Management…
12
5

Primary Partial Absence Atypical

GTC S
absence
myocl
onic,
Atonic
.
First line Valproic acid Carbamazepi Valproic acid Valproic acid.
ne
Lamotrigine Ethusuximide
Phenyt
oin
Valproic
acid
Second line Phenytoin Topiramate Lamotrigin Lamotrigin.
Carbamaze Phenobarbito Clonazepam Clonaze
 Epilepsy-Management…
Surgical methods  Surgical removal of
 For patients whose epileptogenic region
epilepsy results from:  Cutting corpus callosum
 Intracranial tumors to prevent spread of
 Abscesses seizures b/n hemispheres
 Temporal lobe resection
 Cysts or

 Vascular anomalies.

 who are refractory to

medical management
 Status Epilepticus
Status Epilepticus- a condition
characterized by:
– continuous or repetitive
seizure Cause or precipitated
by:
– with impairment of consciousness  Non compliance with
AED(with drawls of
during interictal period, antisezure medication)
– which lasts for more than 30  CNS infections
 Metabolic
minutes
– Generalized seizures that occurs with derangement
– Acute prolonged seizure activity  Tumors,Trauma, Stroke,
out full recovery of consciousness Fever

between attacks
– It is a medical emergency!
 Status Epilepticus-
C/features
Diagnostic Findings
 Patient is having
 EEG
over convulsion  History of epilepsy
 After 30-35 min of
/seizure withdrawal of
uninterrupted the drugs
seizure,_the signs may  Blood tests
become increasingly  Glucose, Electrolytes,
subtle. LFT, RFT .
 Status Epilepticus-Complications
 Hypoxia

 Metabolic acidosis

 Hypotension

 Hyperthermia

 Irreversible neuronal
injury
 Hypoglycemia
 Management
Goals of treatment:
1.Emergency supportive
 To stop the seizures as measures:

quickly as possible.  Keep Airway patent and

 To ensure adequate maintain breathing

 Secure IV line and take blood
cerebral oxygenation
 To maintain the patient
for lab Invn.
 Give glucose IV with Thiamine
in a seizure-free state.
 Take blood for
laboratory
investigation
 Management…
2.Control the seizure with anticonvulsant.
 Diazepam IV 5-10mgIV.

 Phenoytoin 20 mg if seizure continues.

 General anesthesia with phentobarbitol, if seizure

becomes refractory.
 Seizure/Epilepsy-Nursing management
Determine:
 the 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

Seizure/Epilepsy-Nursing mgt…
 Nursing Management- After a Seizure
 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.

 Seizure/Epilepsy-Nursing mgt…
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.
 Nursing Management- During a Seizure
 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.
 Nursing Management…
 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.

 Nursing Management…
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/work, to get married and

establish family.
 Educate patients and families:
 about the diseases and what precautions patient
should take:
 Nursing Management…
 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.
 Swimming ,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
 Nursing Management…
 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

 Able to discuss feelings
 Identifies rights under Federal law
 Headache
Group discussion
1. What is headache
2. Is headache symptom or Disease
3. What is the difference between ache and pain

01/04/2025 Neurologic Disorders 139

 Headaches
• This encompass all aches and pains located in the head
• It is common symptom of neurological disorders
• Mostly result from irritation of meninges and blood
vessels
• Felt by a thalamus
• Interpreted by cerebral cortex

01/04/2025 Neurologic Disorders 140

 Headaches…con’d

• Brain cells do not have nociceptors

• Pain-producing structures in CNS

• Scalp
• Middle meningeal artery
• Proximal segments of the large cerebral arteries
• Sinuses
• Eyes/orbits, Ears, Teeth, Blood vessels

CN V,VII and IX carry pain from these structure

01/04/2025 Neurologic Disorders 141
 Types of Headache
 Primary headaches are those in which headache and its

associated features are the disorder in itself

 occur with no underlying medical causes

 Result from over activity or problem with pain sensitive

structure in the head.

 Secondary headaches are those caused by exogenous

disorders

– occur with underlying causes Ex. Stroke , tumor, infection , etc

– Painful cranial neuropathies and other facial pains

01/04/2025 Neurologic Disorders 142
 A. Secondary Headache Disorders

• Associated with vascular disorders

Subarachnoid hemorrhage
Acute ischemic cerebrovascular disorder
Arteritis
Carotid or vertebral artery pain
Venous thrombosis

01/04/2025 Neurologic Disorders 143

 Secondary Headache Disorders …

• Associated with non-vascular intracranial disorder

• Intracranial infection (e.g. meningitis)
• High/Low CSF pressure
• Brain abscess
• Primary brain tumor
• Associated with non cephalic disorders/infection
• Glaucoma
• Viral rhinitis
• Bacterial infection (sinusitis)
01/04/2025 Neurologic Disorders 144
 Secondary Headache Disorders…
• Associated with head trauma
• Acute post-traumatic headache

• Associated with substance use or withdrawal

• Acute use or exposure

• Chronic use or exposure

• Associated with metabolic disorders

• Hypoxia

• Hypercapnia

• Hypoglycemia

• Post ictal headache

01/04/2025 Neurologic Disorders 145
• Dialysis
 B. PRIMARY HEADACHES

• Disorders in which headache and associated features occur in the

absence of any exogenous cause.
• They are usually recurrent

• Intrinsic dysfunction of the nervous system

• Often results in considerable disability and a decrease in the patient's

quality of life.
• It related to Chemical activity in brain , nerve or blood supply to brain,
muscle surround head
• The most common are :-
– Migraine,

– Tension-type headache, and

01/04/2025 Neurologic Disorders 146
– Cluster headache
 Types of primary headache

01/04/2025 Neurologic Disorders 147

 A. Migraine

• Greek word which means “half head,”

• characterized by periodic and recurrent attacks of severe
headache.
– Intense pounding/ throbbing pain
– This pain is felt on one side of the body

• Migraine pain =felt at anterior and posterior regions

of the head and the upper neck
• It is the second most common cause of 1oheadache(16%)

01/04/2025 Neurologic Disorders 148

 Triggering factors
1. Family history of migraine present in nearly 2/3 of patients.

2. Environmental, dietary and psychological factors.

• Emotional stress , depression

• Altered sleep pattern or sleep deprivation

• Menses , Oral contraceptives

• Caffeine withdrawal
 Foods containing nitrates

 Fermented foods (pasta salads)

 Caffeinated drinks (e.g. soft drinks, tea and coffee)

01/04/2025 Neurologic Disorders 149
 Alcoholic beverages (especially red wine)
 Pathophysiology

1) Vascular theory: In this theory it is said that migraine

and neurological symptoms are results of intracranial
vasoconstriction and extra cranial vasodilatation.
 Cortical ischemia----vasoconstriction affecting the arteries

2) Neuronal theory: a slowly spreading neuronal

depolarization is considered as a cause.
3) Trigeminovascular system abnormality: this theory
says dysfunction of trigeminal nucleus leads to release of
vasoactive neuropeptides resulting in migraine.
01/04/2025 Neurologic Disorders 150
 Trigeminovascular system

• Sensory neurons project to innervate large cerebral

vessels, dura mater, and large venous sinuses
• convergence of the projections from the upper cervical
nerve roots and the trigeminal nerve at the trigeminal
nucleus caudalis
• Fibers from the trigeminal nucleus caudalis ascend to
the thalamus and to the sensory cortex release of
vasoactive neuropeptides, including substance P,
calcitonin gene-related
01/04/2025
peptide, and neurokinin A
Neurologic Disorders 151
• Neurogenic inflammation/ sterile inflammatory response
– Vasodilation (calcitonin gene-related peptide is a potent
vasodilator) and
– plasma protein extravasation
• Neurogenic inflammation: prolongation and intensification of
the pain of migraine
• Neurogenic inflammation may lead to the process of
sensitization.
 Neurons become increasingly responsive to nociceptive
and non-nociceptive stimulation

01/04/2025 Neurologic Disorders 152

01/04/2025 Neurologic Disorders 153
 Trigeminovascular system………..

01/04/2025 Neurologic Disorders 154

 Subtypes of migraine
1. Common migraine /Migraine without Aura
– Do not give any warning signs before the onset of headache.

– It occurs in about 70 to 80% of migraine patients

2. Classic Migraine /migraine with Aura

– Give some warning signs “ called aura”

– 20 to 30% migraine sufferers experience aura.

– The most common aura is visual which includes

• Negative scotoma/ negative visual field defects

– Loss of local awareness

• Positive Scotoma / positive visual field defects

01/04/2025 Neurologic Disorders 155
– Additional structures e.g. Zigzag structure
• The syndrome of Classical migraine has five phases:

1. Prodromal phase: characterized by tiredness, irritability

difficulty in concentrating
2. Aura phase: patients with aura often report visual complaints,
vertigo, aphasia or other neurological deficit before the onset
of the headache(usually1hour)
3. Headache phase – characteristic migraine headache
4. Headache termination – usually occurs within 24 hours
5. Post prodrome phase – feeling of fatigue. Sleepiness and
irritability

01/04/2025 Neurologic Disorders 156

 Clinical Manifestations

 Nausea  Diarrhea
 Photophobia  Fortification spectra
 Lightheadedness  Syncope
 Scalp tenderness  Seizure
 Vomiting  Confusional state
 Visual disturbances
 Vertigo
01/04/2025 Neurologic Disorders 157
 Diagnosis
• Clinical features
• Investigations
IHS diagnostic criteria for migraine
EEG
CT scan
MRI

01/04/2025 Neurologic Disorders 158

 The IHS ( International headache society)diagnostic criteria

 At least five attacks that last 4 - 72 hrs

• At least 2 of the ff xstics: • PLUS==> At least one of

i. Unilateral location; the following occurs:
ii. Throbing /pulsating i. Nausea and/or
quality; vomiting;
iii. Moderate or severe ii. Photophobia and
intensity; iii. Phonophobia
iv. Aggravation by
movement

NB: History, physical examination, and neurologic examination do not

suggest any underlying disease
01/04/2025 Neurologic Disorders 159
 Management
• Three basic approaches to treatment of migraine
1. Avoidance of trigger factors.
2. preventative (prophylactic) medications
3. Abortive treatment

• Treatment Objectives

– Relieve pain

– Prevent recurrences

– Improve quality of life

• Non pharmaclogic

– Patients should be reassured that this is a benign condition.

– They should attempt to identify foods or drinks and other situations,

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which precipitate the attack and try to diminish patterns of tension.
 Pharmacologic

1. Acute treatment, mild attacks:

– First line:-.
• Paracetamol,1000 mg P.O. 4-6 hourly/PN
• Initiate therapy during the attack or at the very onset
of the headache. OR
• Ibuprofen.
• Diclofenac, 50 -100mg PO or IM over day

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 Treatment: Pharmacologic …

2. Antiemetics —Metoclopramide 10 mg, I.V, stat. (used as

an adjunctive or monotherapy)
3. Prevention of early recurrence- add to abortive therapy
to prevent early recurrence.
• Dexamethasone.

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 Non-pharmacological strategies

 Lifestyle changes: Pt. tend to lie down in a dark, quiet room,

 Sleep: Maintain consistent sleep patterns and try not

to get too much or too little.

 Exercise:

 Eating: Eat regular meals, and do not skip meals

 Reduce stress

 Improve posture: Pay special attention to how you

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hold your neck and shoulders.
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 B. Tension-Type Headache

• Headache that has steady ache ( muscle contraction)

• Also called Muscle Contraction Headache
• Most common type of primary headache (63%)
• Characterized by a steady, constant feeling of pressure
that usually begins in the forehead
• Band like (“A weight on top of my head”)
 Emotional or physical stress may cause contraction of
the muscle in the neck and scalp, resulting in tension
headache
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 Pathogenesis
• Emotional tension leads to muscle tension and hence to
headache

• Increased myofascial (TMD) pain sensitivity

• Psychological Factors

– Anxiety, depression, anger, and hostility

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 Clinical presentation be undisturbed.

– Headache may be episodic or – Not associated with nausea and

chronic (present >15 days per vomiting

month) – Much less commonly associated

– Begin at any age with light and sound sensitivity

 TTH are completely without
– Tight band around the head, a
accompanying features such as:
sense of pressure, or a bursting
 Nausea, vomiting,
sensation  Photophobia,
 Phonophobia,
– Despite the complaint of a
 Throbbing, and
constant headache, sleep may

01/04/2025 Neurologic DisordersAggravation with movement., 166
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 Treatment
• Reassurance
• Relaxation of the scalp
• Mild TTH  aspirin or acetaminophen
• NSAIDs, such as ibuprofen,
• Most effective prophylactic drug is amitriptyline
– The usual dose is 50 to 150 mg/day, but higher doses
may be needed

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 C. Cluster headache
 It is the most painful  Characterized by
recurrent headache (10/10) – severe one-sided headache
in severity – Eye tearing or redness
 It can be :- (90% of people),
– Episodic- attacks of pain – running of one nostril
occur in periods lasting 7 (84%),
days to 1 year separated – sweating or flushing
by pain-free periods (59%), or swelling of the
lasting 1 month or longer eyelid which occur on
– Chronic -attacks of pain the same side of the head
occur for more than 1 as :-
year without remission or • Intense,
with remissions lasting • stabbing pain, usually
less than 1 month Neurologic Disorders behind one eye
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 Triggering factors for cluster type headache

 The most reliable Trigger is alcohol, and beer.

 Family history of migraine (18%).

 Nitrites, vasodilators, and histamines may

precipitate cluster headaches.

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 Clinical Features

• Common in male
• Onset typically begins in the third decade of life
• Periodicity is a cardinal feature of cluster headache
• Commonly one or two attack per year
• During a cluster( 1-3 attacks in 24 hours)
• Onset during the night or 1 to 2 hours after falling asleep
• Pain intensifies very rapidly(peak 5-10min, duration
45min-2 hrs )
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 C/m cont…
• Pain is often unilateral
– pain felt retro-orbital and temporal regions (upper syndrome)

– Pain may be maximal in the cheek or jaw (lower

syndrome).

• Onset is usually abrupt

• Tension and discomfort in the same side limbs and

neck, either during the attack or just preceding it.

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 C/m of luster headache..

• Aura (rarely)

• Patient avoid the recumbent position

• Overflow of tear, conjectival injection

• Unilateral Profuse sweating and facial flushing

• Ptosis and miosis on the side of the pain may occur.

• Facial swelling, most often periorbital,

Neurologic Disorders
• The nostril on the side of the pain is generally blocked
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 Cluster headache

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 Treatment

• The most satisfactory treatment is the administration

of drugs to prevent cluster attacks until the attack is
over
• Acute attack treatment
– oxygen inhalation.
• This should be given as 100% oxygen at 10–12
L/min for 15–20 min.
– Sumatriptan 6 mg SC has rapid onset (usually
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 prophylaxis

• CCB- verapamil 80 to 160 mg three times a

day ,it is first line treatment with fewer side
effect
• chronic cluster headache
– Lithium carbonate, 300 mg three times a day

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 Summary

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