• Neuro Part 2 ○ 2 types

○ Julie Mann, NP  ischemic:

○ N145  caused by a thrombus or embolus
• Case Study  hemorrhagic:
○ Mr. Brown is a 76 year old man with a pmh  caused by a rupture of a blood
significant for HTN and high cholesterol. He vessel with bleeding into the brain
takes an ACE Inhibitor and a statin and is tissue
well controlled on these medications. He  Atherosclerotic plaque builds in
goes to church on sunday morning and has brain blood vessel, thins, ruptures.
trouble reading the bulletin, a few minutes
later he loses his balance and falls to the
floor.
○ What might be going on with Mr. Brown?
 Stroke
 HTN and high cholesterol puts at risk
for stroke.
○ Why would he have trouble reading?
 Clot in brain.
○ Why would he lose his balance?
 Stroke effecting areas of brain.
• Mr. Brown
○ A nurse a few pews back a nurse witnesses
his fall and is first on the scene.
○ What should he do first?
 ABC - airway, breathing, circulation.
 LOC
○ What should be assessed? ○ Mr. Brown makes it into the hospital and is
○ What would you expect to find? found to have this heart rhythm:
• Cerebral Vascular Accident
○ An acute focal neurological deficit due to a
disturbance in the blood vessels supplying
the brain.

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  Irregularly irregular rhythm with no P-
wave. Atrial fibulation. Firing at random
intervals, heart quivers instead of
pumping properly.
○ What is the connection between this
rhythm and his stroke?
 In the example pic below some blood
stays in the atrium, clots, and the clot
floats up to the brain.
• Types of Ischemic Stroke
○ Cardiogenic Embolic Stroke:
 moving blood clot travels to brain;
usually lodges at a bifurcation (middle
cerebral artery)
 Heart originating.
○ Large Vessel (Thrombotic) Stroke:
 atherosclerotic lesion/plaques form at
an arterial bifurcations.
○ Small Vessel (Lacunar) Infarct:
 small infarcts that occur deep in
noncortical parts of brain and brain
stem; occlusion from penetrating
branches of cerebral arteries.
 Often from atherosclerotic plaques.
 May send off small clots downstream.
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• Ischemic Stroke
○ Stroke evolution: central area of dead or
dying tissue surrounded by ischemic band
of at risk cells (penumbra [halo]) -
immediate
○ survival of this tissue depends on:
• timely return of circulation
• amount of toxic chemicals from dead
cells
• amount of cerebral edema
 Pressure on healthy cells.
• alterations in local blood flow
• Manifestations of Acute Stroke
○ Depends on Cerebral Artery affected and
amount of collateral circulation.
○ See table 51-6 in text (p. 1321)
○ usually sudden onset, focal (one portion of
brain), and one-sided
○ Most common symptoms to all are:
unilateral weakness, unilateral numbness ,
vision loss in one eye or one side, language
disturbance (slurred speech to aphasia
[can't speak at all]), and sudden
unexplained imbalance or ataxia.
• Transient Ischemic Attacks (TIA)
○ Focal cerebral neurological deficits lasting
less than 24 hours.
• Symptoms will resolve
○ Brain angina, get ischemic.
○ A zone of penumbra without central infarct.
○ If have one, high risk for having another,
can progress to a stroke.
• Stroke Risk Factors
○ Unmodifiable Factors
• Age
• Sex (Male)
• Race (African American, Caucasian)
• Heredity
• Migraines (according to teacher)
○ Modifiable Risk Factors
• HTN, DM, Smoking
• Hyperlipidemia
• Heart Disease (a-fib, wall motion
defects)
• Carotid disease
• Coagulation disorders
• Heavy ETOH use
• Cocaine use (vasoactive substance--
>vasospasm)
• Case #2
○ Mr. Roberts is an 83 y/o man with a pmh
significant for htn and colon CA. He was
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 helping serve lunch at the local VFW hall
when he fell to the floor and became
unresponsive. When EMS arrived some
witnesses told the paramedics that he had
complained of HA a little while before he
collapsed.
○ Why did Mr. Robert’s collapse?
• Preceding HA --> hemorrhagic stroke.
○ Is it likely he has the same issue as Mr.
Brown?
• Possibly, similar risk factors.
○ What are you concerned about related to
his symptoms?
• Hemorrhagic Stroke
○ rupture of blood vessel, hemorrhage into
brain tissue, focal hematoma
○ sometimes intraventricular hemorrhage,
edema, compression of brain contents
leading to spasm of surrounding blood
vessels and ischemia to surrounding tissue.
• no room for growth, increased pressure
○ Occurs suddenly
against skull
○ HA and vomiting common at onset
○ Focal symptoms depend on vessel involved
(larger vessel worse, occludes more further
down)
○ hemorrhage and subsequent edema puts
pressure on brain
○ rapid progression to coma and frequently to
death.
• Case #3
○ Lola is a 33 y/o Caucasian woman with no
significant pmh. She c/o frequent periods of
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 fatigue accompanied by vertigo, and some
numbness and tingling in her face. She
states when these episodes occur she is
often really clumsy.
○ What might be causing Lola’s symptoms?
• MS, recreational drugs.
○ What other questions might you ask her?
• How does episode effects life? Major
impact on life, job. What happens to
you during episode.
• What happens when starts, triggers,
and alleviating factors.
• How to maintain best quality of life,
sleeping, social life, work life,
interpersonal life, on what levels. • MS Lesion
• Multiple Sclerosis ○ plaques - hard, sharp-edged demyelinated
○ Demyelinating disorder characterized by or sclerotic patch in the CNS.
inflammation and selective destruction of ○ represent the end of the breakdown of the
the CNS myelin. myelin sheath and are called plaques
○ affects the white matter of the brain, spinal ○ plaques contain myelin proteins along with
cord, and optic nerve proteolytic enzymes (break down myelin
○ No affect on the PNS, doesn’t become a sheath), macrophages, lymphocytes, and
systemic condition plasma cells.
○ Immune mediated disorder (immune
system responds to a protein in the CNS)

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• Who’s at risk?
○ European ancestry
○ High rates in Europe, North America, and
Canada
○ More common in northern latitudes
○ Not found in certain ethnic groups
• Native Americans, Africans, certain
Asians.
○ increased risk if first degree relatives have
MS (15X more likely)
○ 1st signs generally b/t 20s-30s.
• Manifestations
○ area’s often affected (can't send messages
properly through demylinated neurons)
• optic nerve (most common, double
vision)
• corticobulbar tracts (speech &
swallowing)
• corticospinal tracts (muscle strength)
• cerebellar tracts (balance)
• medial longitudinal fasciculus
(conjugate gaze function of
extraoccular muscles, where gaze lies)
• posterior columns of the spinal cord
(position and vibratory sense)
• Manifestations
○ depend on extent and location of
lesion/plaques.
○ symptoms last for days to several weeks
with periods of remissions
• Some have same level remissions,
some have more severe remissions
each time it occurs.
○ Psychological manifestations: mood swings,
depression, euphoria, inattentiveness,
forgetfulness, apathy and loss of memory.
○ Fatigue (everything becomes harder to do
d/t demyelization)
• Case #4
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○ Steve is a 30 y/o man with no significant
pmh who presents with c/o progressive
weakness and diplopia (double vision).
○ What do you notice about his picture?
• Ptosis, corner of mouth droops.
○ What might be going on with Steve?
• Myasthenia Gravis
• Myasthenia Gravis
○ disorder of the transmission at the
neuromuscular junction
○ disrupts communication between motor
neuron and the innervated muscle cell
○ autoimmune disease
○ antibody-mediated loss of acetylycholine
receptors in the neuromuscular junction.
• Messages do not transduce.
○ impairs signal transmission
• Clinical Manifestations
○ Manifests on one side at start, progresses
bilaterally.
○ muscle weakness and easy muscle fatigue
○ most commonly affects the eyes and
periorbital muscles (ptosis[drooping eyelid],
diplopia [double vision])
○ progresses from ocular muscle weakness to
generalized weakness to resp. muscle
weakness
○ can exacerbate into myasthenic crisis
during stress
• Rapidly lose muscle strength, and
rapidly effects the respiratory muscles.
Need to support airway.
○ Therapy: immunosuppressant
• Case #5
○ Mr. Hide is a 67 y/o male with no pertinent
pmh. He presents for his routine physical
exam and the NP notes he has a tremor in
his left hand. Upon further examination the
NP finds slowness of originating movement
and rigidity in his ROM.
○ What concerns you about the NP findings?
• Tremor
• Difficulty in moving, falls, doing things.
○ What disease process might be going on?
• Parkinson Disease
○ degenerative disorder of the basal ganglia
○ patho largely unknown, suggests genetic,
viral, or toxic causes (can occur in clusters).
○ usually begins after 50 years of age
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 ○ dopamine is depleted
○ dopamine receptors are destroyed
○ imbalance in the dopaminergic (inhibitory)
and cholinergic (excitatory) activity
○ Excess cholinergic activity causing the
symptoms we see.
○ Occurs more in males.
• Clinical Manifestations
○ Tremor:
• mainly affects hands and feet (pill
rolling tremor); head, neck, face, lips,
and tongue, or jaw
• rhythmic, alternating flexion and
contraction
○ Rigidity:
• found during PROM (passive range of
motion), jerky, ratchet-like movements
• can result in flexion contractions,
muscles tighten and unable to extend.
exhaustion
○ Bradykinesia:
• slowness in starting and performing
movements.
• Difficult to initiate walking, hard to get
○ Early: Infrequent blinking (dry eyes), lack of
momentum started, turning is hard.
facial expression, deliberateness of speech,
• Parkinson Symptoms
resting pill-rolling tremor one hand
○ Mid: Progressive Rigidity, slowness,
difficulty originating movement, stooped
posture, slow shuffling gait, resting tremor
of jaw, tongue, lips, and limbs
○ Late: Severe postural instability, urinary
retention, orthostatic hypotension (d/t
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 vasomotor interactions), paranoia with
visual hallucinations, delirium, dementia
• The Good News
• Case #6
○ Tommy is a 15 year old boy who goes to the
community pool to meet up with his
friends. They start trying to impress each
other and do “crazy ways” to jump into the
pool. Tommy’s jump wasn’t so successful
and he ends up hitting his head on the
bottom of the pool.
○ What are our immediate concerns for
Tommy?
• Drowning,
○ What do you do first?
• cervical spine precautions (backboard
and neck brace in water before moving
out of pool) Jaw thrust
• Spinal Cord Injuries (SCI)
○ any damage to the neural part of the spinal
cord.
○ Most common causes are MVA (motor
vehicle accidents), falls, violence (GSW Gun
Shot Wound), and recreational sports
○ most injuries result from compressive force
(on vertebrae, impact cord) or bending
injuries (cervical spine injury, hyperextend
neck).
• immediately after SCI
○ Spinal Shock:
• characterized by flaccid paralysis and
loss of reflexes below injury; loss of
sensation below injury; and loss of
bowel and bladder function.
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 • loss of systemic vasomotor tone:
vasodilation, increased venous
capacity, hypotension.
• may last for days or weeks (need
medical support)
• in general the higher the injury the
greater the affect
• SCI
○ Primary Injury: occurs at time of mechanical
injury.
• small hemorrhages in the gray matter
of the cord develop
• edema in the white matter
• both lead to neural tissue necrosis
○ Secondary Injury
• follows primary and promotes spread of
injury on surrounding tissue.
• the release of vasoactive substances
(NE, histamine, & dopamine) from
wound tissue cause vasospasm and
impedes blood flow to neighboring
areas damaging more tissue.

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• Read pg 1291-95!!!
○ Focus on: motor changes, reflexes lost
below site of injury, vasomotor (temp reg).

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