Unit 5: NEUROLOGIC NERVOUS SYSTEM o Immune system system heats

DISORDER up as response in the sinus area

- Nueropepetides are being
• Control center
released
• Regulate the body systems o Pressure to cranial arteries and
• Associates to thinking, movements and veins and muscles of neck and
emotions head
2 Major Division o Nociceptor-pain receptor
o Throbbing pain of headache
• Central Nervous System
o Brain PRIMARY HEADACHE
o Spinal Migraine
• Peripheral Nervous System
o Nerves: • Migraine is common, recurrent, primary
▪ Sensory Nerves headache of moderate to severe
▪ Motor Nerves intensity that interferes with normal
➢ Voluntary functioning and is associated with GI,
(somatic) neurologic and autonomic symptoms.
➢ Involunatary
Trigeminal nerve
(Autonamic)
Cranial v is activated → releases neuropeptide
2 division in Involuntary
1. Vasoactive inhibitory peptide
• Sympathetic NS = Fight/flight response 2. Subs p
• Parasympathetic NS = Rest/Digest 3. Calcitonin gene related peptide –
painful neurogenic inflammation in
meningeal vasculature
TOPIC 1
4. Mast cell degranulation
HEADACHE 5. Plasma protein extravasation
6. Vasodilation
NOTES: 7. Activation of nociceptors
Primary Headache – it’s the main condition Result migraine

• Types: Migraine, Cluster and Tension PATHOPHYSIOLOGY (Migraine)

Secondary Headache – Cause by health • Defect in the activity of neuronal

problems calcium channels mediating
neurotransmitter release in the
• Dehydration brainstem areas that modulate cerebral
• Caffeine withdrawal vascular tone and nociception.
• Injury • It will lead to vasodilation of intercranial
• Heart Disease extracerebral blood vessels with
• Sinus infection activation of the trigeminovascular
system.
Sinus Infection
• Heritability of migraine.
• Infection on sinus area
 o Migraine triggers may be
modulators of the genetic set
point that predisposes to
migraine headache
• Serotonin receptors
o Acute antimigraine drugs such
as ergot alkaloids and triptan
derivative are agonist of
vascular and neuronal 5HT1
receptor subtypes.
o It will result in vasoconstriction
and inhibition of vasoactive
neuropeptide release and pain
signal transmission
CLINICAL MANIFESTATION (Migraine)
• Recurring unilateral episodes of
throbbing head pain.
• Associated with nausea, vomiting and
sensitivity to light, sound and/ or
movement.
• Migraine aura (classic migraine)
o A recurring headache that
strikes after or at the same time
as sensory disturbances.
• Premonitory symptoms:
o Neurological (Phonophobia,
photophobia, hypersomnia
difficulty in concentrating)
o Psychological (anxiety,
depression, euphoria,
irritability, drowsiness,
hyperactivity, restlessness)
o Autonomic (polyuria, diarrhea,
constipation)
o Constitutional (stiff neck,
yawning, thirst, food cravings,
anorexia
CLINICAL ASSESSMENT (Migraine)
• Comprehensive headache history
• Headache evaluation
o Stable pattern of headache
o Absences of daily headache
o Positive family history for
migraines
• General medical and neurologic
examination
• Diagnostic and laboratory assessment
• Neuroimaging
NONPHARMACOLOGIC (Migraine)
• Application of ice in head
• Period of rest or sleep, usually in
darkquiet environment.
• Behavioral intervention
PHARMACOLOGIC INTERVENTION (Migraine)
• Pretreatment with antiemetics.
• First line treatment for mild to
moderate migraine attacks is simple
analgesics and NSAIDs.
• Use of ergot alkaloids and derivatives
• Serotonin receptor agonis
• Prophylactic therapy for recurring
migraine attacks.
• Preventive therapy for headache that
occurs in a predictable pattern
TENSION-TYPE HEADACHE
• It is the most common type of primary
headache and more common in women
than men.
• Pain is usually mild to moderate,
bilateral, non-pulsatile.
• Episodic headaches may become
chronic.
PATHOPHYSIOLOGY (TENSION-TYPE HEADACHE)
• It can originate from myofascial factors
and peripheral sensitization of
nociceptors
• Involvement of central mechanism.
• Activation of supraspinal pain
perception structures
CLINICAL MANIFESTATION (TENSION-TYPE
HEADACHE)
 • Premonitory symptoms and aura are
absent
• Pain is usually mild to moderate,
bilateral, non pulsatile and in the
frontal and temporal areas, but
occipital and parietal areas can also be
affected
• Mild photophobia or phonophobia may
occur.
• Pericranial or cervical muscles may have
tender spots or localized nodules in
some patients
TOPIC 2:
PAIN
PAIN MANAGMENT
• Pain is an unpleasant, subjective,
sensory and emotional experience
assocaiated with actual or potential
tissue damage or described in terms of
such damage.
Note:
“ay napaso siya” = aray masakit HAHAHHAHHA
Noxious signals → impulse → spinal cord →
brain → interprets → sends back signals on
how to response
PATHOPHYSIOLOGY (pain)
• Nociceptors are pain sensing nerve
cells. It can be located in either somatic
or visceral
• It will propagate the information to the
spinal cord nearby.
• The action potential will trigger the
release pain neuro transmitter
(substance P).
• It will ascends to higher centers.
• The thalmus acts as relay station and
passes the impulses to the central
structure.
• Body will modulate the pain.
o Endogenous opiate system will
be activated.
o Neurotransmitter such as
enkephalins, dynorphins and B-
endorphins will bind to the
receptors mu, delta and kappa
NEUROPATHIC PAIN
• It is resulted from nerve damage. E.g.
o Postherpetic neuralgia
o Diabetic neuropathy
• Acute pain is usually a nociceptive but
can be neuropathic
• Chronic pain can be both neuropathic
and functional pain, for example, a pain
that persist after the healing of acute
injury
FUNCTIONAL PAIN
• It refers to the abnormal operation of
the nervous system E.g.
o Fibromyalgia
o Irritable bowel syndrome
o Tension-type headache
CLINICAL MANIFESTATION (pain)
• Patient can have a distress from trauma
or appear to have no noticeable
suffering
• Acute pain
o Sharp or dull, burning, shock-
like tingling, shooting radiating,
fluctuating intensity, varying
location and occur in a timely
relationship with an obvious
noxious stimulus
• Acute pain can cause HTN, tachycardia,
diaphoresis, mydriasis and palor.
• Acute pain there is no relation with
comorbid conditions unlike chronic
pain, there is.
• Chronic pain occurs without a timely
relationship with a noxious stimulus.
CLINICAL ASSESSMENT (pain)
• Patient medical history
• Pain Scale
• Blood Chemistry
• PQRST characteristic – (Provocation/
palliation) (quality/quantity)
(region/radiation) (severity/scale)
(timing
• Medications
Note:
PainHS (blood chemistry) – light measurement
tool known as hyperspectral imaging analysis to
identify structure of what pain looks like in
blood cells
Pain Scale
CLINICAL INTERVENTION (pain)
• Non-opioid agents
o Given for mild to moderate pain
o Fewer side effects (GI
problems)
• Opioid agents
o Given for severe pain at high
dose
o Partial agonist and antagonist-
selectivity with the pain
receptor site.
o Might exhibit allergic reaction.
• Intrathecal and epidural opioids are
often administered with patient-
controlled analgesia.
o Safe and effective (lesser side
effect)
• Morphine is the first line agent for
moderate to severe pain.
o Cause respiratory depression
that why it’s given with
naxolone
DESIRED OUTCOMES (pain)
• Minimize the pain
• Provide reasonable comfort
Topic 3
PARKINSON’S DISEASE genetic cause
(mutation)
Note:
Substantia nigra→ dopamine producing neuron
(degenerates) → decrease amount of dopamine
Substantia nigra is part of basal ganglia
basal ganglia connected to motor cortex
gene mutate in parkinson’s disease –
Phosphatase and tensin homologue induced
kinase 1 & Parkin Parkinson Juvenile Disease
Protein 2 (Pink1 & Parkin)
Lewy body – eosinophilic, alpha-synuclein
PARKINSON’S DISEASE
• Parkinson’s disease has highly
characteristic neuropathologic findings
and clinical presentation. This includes:
o Motor deficits
o Mental deterioration
PATHOPHYSIOLOGY (PARKINSON’S DISEASE)
• 2 known hallmarks in the substantia
nigra pars compacta:
1. Loss of neurons
2. Presence of lewy bodies -
Alpha-synuclein
 • The degree of nigrostriatal dopamine
loss has good correlation with loss and
severity of motor function.
• The inhibition of thalmus is resulted
from inactivation of dopamine-1 and
dopamine2
• The tremor exhibited by the patients
with Parkinson’s disease is due to
degeneration of nigrostriatal dopamine
neurons
COMPLICATION (PARKINSON’S DISEASE)
• Thinking difficulties
o Cognitive problems such as
dementia occurs in the later
stage of Parkinson’s disease.
CLINICAL ASSESSMENT (PARKINSON’S DISEASE)
• Depression and emotional changes
o In the very early stage, it is
usually developed.
o Receiving treatment for
depression can make it easier
to handle the challenges of
Parkinson’s disease.
• Swallowing problems
o Saliva may accumulate in your
mouth due to slowed
swallowing, leading to drooling.
• Chewing and eating problems
PHARMACOLOGIC INTERVENTION
o Late-stage of PD affects the
(PARKINSON’S DISEASE)
muscle in the mouth which
makes chewing difficult.
o It can lead to choking and poor
nutrition.
• Sleep problems and sleep disorders
o People with PD often frequently
waking up throughout the
night, waking early or falling
asleep during the day
• Bladder problems and constipation
CLINICAL MANIFESTATION (PARKINSON’S
DISEASE)
• Initial symptom is sensory but as the
disease progresses, there are one or
more classic symptoms presents.
o Resting tremor
o Rigidity
o Bradykinesia
o Postural instability
• Resting tremor
o Tremor is present mostly in the
hands and sometimes
characterize as pin- rolling
• Muscle rigidity
o Increase muscle resistance to
passive range of motion.
• Intellectual deterioration
• Medical history
o Medication that maybe a drug-
induced parkinsonism
• Neuroimaging
o SPECT scan aka Dopamine
transporter (DAT Scan)
• Deep Brain Stimulation (DBS)
o Placing electrodes that are
surgically implanted in the
brain.
• Carbidopa-Levodopa
o Levodapa protects the
conversion of dopamine
outside the brain.
• Carbidopa-Levodopa infusion
o It is administered through the
feeding tube.
• Dopamine agonists
o Mimics the dopamine in the
brain.
• MAO-B inhibitors
o Help prevents the breakdown
of brain dopamine by inhibiting
the enzyme MAO B.
 • COMT inhibitors
o It prolongs the effect of
levodopa therapy by blocking
an enzyme that breaks down
dopamine
• Anticholinergics
o This medication help control
the tremor associated with
Parkinson’s disease.
• Amantadine
o Provide short-term relief of
symptoms of mild, earlystage
Parkinson’s disease
SURGICAL PROCEDURES (PARKINSON’S
DISEASE)
• DBS
o Deep Brain stimulation- implant
electrodes into specific part of
the brain.
o The electric pulses from the
heart is send to the brain to
reduce Parkinson’s disease
symptoms
NONPHARMACOLOGIC INTERVENTION
(PARKINSON’S DISEASE)
• Speech-language pathologist
• Diet
o Food high in fiber and drinking
an adequate amount of fluids
can help prevent constipation
• Exercise
o Increase muscle strength,
flexibility and balance
o Improve well-being and reduce
depression or anxiety.
ALTERNATIVE INTERVENTION (PARKINSON’S
DISEASE)
• Massage
o Reduce muscle tension and
promote relaxation
• Tai chi
o It is an ancient form of Chinese
exercise, tai chi employs slow,
flowing motions that may
improve flexibility, balance and
muscle strength
• Yoga
o It can increase flexibility and
balance.
• Alexander technique
o It focuses on the muscle
posture, balance and thinking
about how you use muscles and
reduce muscle tension.
• Meditation
o It can reflect and focus your
mind on an idea or image.
o It may reduce stress and pain
and improve your sense of well-
being
• Pet therapy
o Increase the flexibility and
movement and improve your
emotional health.
Topic 4
Epilepsy
Note:
Too much Excitatory – Excitatory NT:
Glutamate
Receptor of Glutamate: N-methyl-D-aspartate
receptor
• What happened if Epilepsy is too much
Excitatory? Fast/ Long lasting activation
Ca comes in
Too little inhibition
Inhibitor Nt: GABA
Rec. of GABA: GABA Receptor
 • It is a chronic disorder that causes
unprovoked, recurrent unprovoked
seizures.
o Seizures is a sudden rush of
electrical activity.
• There are 2 main types of seizures:
o General seizures- whole brain
o Focal or partial seizures- one
part of the brain
• It affects 65 million worldwide.
• It can affect everyone but it is common
in young children and older adults. It
occurs slightly more in male than
females.
ETIOLOGY (EPILEPSY)
• High fever
• Head trauma
• Very low blood sugar
• Alcohol withdrawal
• Genetic or Development disorders or
neurological disease
CLINICAL MANIFESTATION (EPILEPSY)
• Symptoms may vary according to type
of seizure.
o Focal (partial) Seizure
o Simple (partial) seizure that
didn’t loss the consciousness of
the patient. It includes:
▪ Changes in the sense of
taste, smell, sight,
hearing or touch.
▪ Dizziness with the
tingling and twitching
sensation of the limbs
o Complex partial seizure which
involves the loss of awareness.
It includes the:
▪ Staring blankly
▪ Unresponsiveness
▪ Performing repetitive
movements
Note:
Simple partial seizure – conscious
Complex partial seizure - unconscious
• Generalized seizures
o Absence seizures
▪ Aka petit mal seizure
which involves stare
blank, lip smacking,
repetitive movements
and usually short loss of
awareness.
o Tonic seizures
▪ muscle stiffness.
o Atonic seizures
▪ Loss of muscle control
and cause sudden
falling down.
o Clonic seizures
▪ repeated, jerky muscle
movement of face, neck
and arms.
o Myoclonic seizures
▪ Spontaneous quick
twitch of arms and legs.
o Tonic-clonic seizures
▪ Aka Grand mal seizures.
▪ Causes stiffening and
shaking of body
▪ Loss of bladder or
bowel control
▪ Biting of tongue
▪ Loss of consciousness
▪ Can’t remember what
happened or you feel
slightly ill for few hours.
BEHAVIORAL CONNECTION (EPILEPSY)
• Children with epilepsy tend to have
more learning and behavioral problems.
o About 15-35% has intellectual
disabilities
 • Some people experience a change in
behavior in the minutes or hours before
the seizure.
• They are show inattentiveness,
irritability, hyperactivity and
aggressiveness
TRIGGERS OF EPILEPSY
• Lack of sleep
• Illness or fever
• Stress
• Bright lights, flashing lights or patterns
• Caffeine, alcohol, medications or drugs.
• Skipping meals, overeating or eat a
specific food
CLINICAL ASSESSMENT (EPILEPSY)
• Medical history
• Neurological examination
o Examine the motor abilities and
mental functioning
• EEG (Electroencephalogram)
o Most common used test for
epilepsy
o The changes in normal brain
wave patterns are common in
epileptic patients, with or
without seizures.
• Imaging test to check the presence of
tumor and other abnormalities
o CT scan
DIETARY RECCOMMENDATION (EPILEPSY)
o MRI
o PET
o Single-photon emission
computerized tomography
LABORATORY ASSESSMENT (EPILEPSY)
• Blood Chemistry
o Check the signs of infectious
disease
o Monitor the liver and kidney
function
o Monitor the glucose level
CLINICAL MANAGEMENT (EPILEPSY)
• Vagus nerve stimulator
o Invasive procedure.
o It gives electric stimulation that
runs through your neck to
prevent seizures.
• Ketogenic Diet
o Provides high fat and low
carbohydrate diet
• Keeping a journal
• Brain Surgery (Resection)
o The area of the brain that
causes seizure activity can be
removed or altered
• Anti-epileptic (anti-convulsant) drugs
o To reduce the episode of
seizure
o Levetiracetam, Lamotrigine,
Topimirate, VPA,
Carbamazepine and
Ethosuximide
• Ketogenic Diet
o The goal is to force the body to
use fat for energy instead of
glucose.
• Modified Atkins Diet
o This diet is also high fat and
involves a controlled carb
intake.
• The common side effect is constipation
due to low in fiber and high fat diet.
• Medical alert bracelet
CLINICAL MANAGEMENT (EPILEPSY)
• No cure for epilepsy only management
with medications and other non-
pharmacologic strategies.
• Yoga and other stress relieving
therapies.
• Several complementary therapies might
work for them.
o Be cautious about reducing or
stop taking your medication.
Consult your family doctor with
regards to that matter.
STATUS EPILEPTICUS
• Status Epilepticus means continuous
state of seizure.
• It is a medical emergency when a
seizure hits the 5 min mark.
• There are 2 main forms of Status
epilepticus, the convulsive and
nonconvulsive type
• Convulsive type:
o more common and dangerous.
o involves tonic-clonic and
sometime referred as grand mal
• Non-convulsive type:
o “Epileptic twilight” state
o Doesn’t lose the consciousness
• Children under age 15 who have
seizures brought on by high fever.
• Adults over 40, will more likely
experience stroke.
CAUSES of SE/STATUS EPILEPTICUS
• Low blood sugar
• HIV
• Head trauma
• Heavy alcohol or drug use
• Kidney or liver failure
CLINICAL ASSESSMENT (STATUS EPILEPTICUS)
• EEG
• Blood chemistry
• Urinalysis
• CT scan
• Chest X-ray
CLINICAL MANAGEMENT (STATUS EPILEPTICUS)
• First line treatment at home:
o Protect the head of the patient
o Move away from the danger
o Resuscitate when needed
o Give emergency medication:
▪ Midazolam- buccal
administration
▪ Diazepam- rectal
administration
• Call an ambulance
• First line treatment at hospital:
o High Oxygen concentration
followed by intubation
o Cardiac and Respiratory
assessment
o Diazepam IV or Lorazepam IV to
suppress seizure activity
• Individual care plan:
o States when the medication will
use.
o States how much should be
given
o States the necessary steps
should be taken afterward
ACUTE MANAGEMENT OF TRAUMATIC BRAIN
INJURY
• Head injury can be defined as any
alteration in mental or physical
functioning related to blow to the head.
• Loss consciousness does not need to
occur
• Traumatic brain injury is a leading cause
of death and disability in trauma
patients
GLASGOW COMA SCALE SCORE
• Generate numerical summed score for
eye, motor and verbal abilities.
 • 13-15 - Mild Injury o The total intercranial volume is
• 9-12 - Moderate Injury a sum of brain tissue, cerebral
• > 8 - Severe Injury spinal fluid, venous blood and
arterial blood.

CLINCAL ASSESSMENT (BRAIN INJURY)

• Bedside cognitive testing- is to

measures the patient’s level of
consciousness, attention and
orientation.
• Imaging test
• EEG

LABORATORY ASSESSMENT (BRAIN INJURY)

CLINICAL MANIFESTATION (BRAIN INJURY)
• Sodium levels
• Bruising or bleeding on the head and • Magnesium levels
scalp • Coagulation studies
• Blood in the ear canal • Blood alcohol
• Anosmia – due to shearing of the • Renal function test and Creatinine
olfactory nerves at the cribriform plate. kinase levels
• Abnormal Postresuscitation pupillary • Neuron-specific enolase and protein S-
reactivity 100B
• Isolated internuclear opthalmoplegia
CLINICAL INTERVENTION (BRAIN INJURY)
secondary to traumatic brain stem
injuries • Management of intercranial pressure
• Cranial nerve VI and VII palsy • Hypertonicity
• Hearing loss • Surgical evacuation of Subdural
• Dysphagia Hematomas
• Focal motor findings

PATHOPHYSIOLOGY (BRAIN INJURY)

• Gross structural changes in head injury.

o Skull fracture (Simple linear
fashion or complicated
depressed manner)
▪ Bone fragments
• Neuronal loss
o Loss of neuron from dorsal
thalmus
• Neurochemical changes
o Catecholamine surges in plasma
and CSF
• Monro-kellie hypothesis