Transcript Acid-Base Imbalance

Neurological
Disorders
Structural Organization
Brainstem & Cerebellum
Cerebral
hemispheres
Spinal and Cranial
Spinal Cord
Nervous System Function
Sensory Inputs
afferent
Brain:
Central
Processing Unit
efferent
Secretion
Movement
Sensory Tracts
anterolateral
dorsal
Major Sensory Tracts

Anterolateral
(Spinothalamic)



crosses
immediately in the
cord
sensation is poorly
localized
itch, pain, temp

Dorsal column



ipsilateral until
medulla, then
crosses
sensation is well
localized
touch, vibration,
pressure,
Major Motor Tracts

Lateral Corticospinal



crosses at medulla
innervates distal
muscles
fine motor control

Medial Tracts



some tracts cross
at medulla, some
don’t
innervates axial
muscles
balance, gross
motor
How Do Neurons Communicate?
dendrite
axon
terminal
axon
synapse
postsynaptic
neuron
Neurotransmitter Classes

Acetylcholine

Amines (DA, NE, E, 5HT, histamine)

Amino acids (glutamate, GABA, glycine)

Purines (adenosine)

Gases (nitric oxide)

Neuropeptides
(Sub P, endorphins, AII, oxytocin, many others)
Head Trauma / Bleeds

Focal: localized

Polar: acceleration-deceleration

Diffuse: widespread disruption
Determinants
of Intracranial Pressure

Three space occupying components




Brain
CSF
Blood
Compensation for Increased ICP


CSF shunt to spinal cord
Hyperventilation leading to vasoconstriction
Causes of Increased ICP

Brain infection

Rupture of blood vessels

Hydrocephalus

F & E imbalances

Head Injury – most common
Types of Injury
 Primary
injury
 Secondary
injury
Pathophysiology
of Secondary Injury
Ischemia
Release of
glutamate
ATP deficiency
Na+, Ca++ in cell
“excitotoxin”
cell damage
vasospasm
platelet plug
Activation of
phospholipases
free radicals
prostaglandins
thromboxanes
mitochondria
dysfunction
Compensation for Increased ICP
Brain Swelling
CSF shunted
to spinal cord
CSF in brain
ventricles
ICP
Hyperventilation
PaCO2
Cerebral vasoconstriction
ICP
Blood in brain
ICP
Progression of S/S of Increasing ICP

Mild to moderate
Headache, LOC,
projectile vomiting,
localized pain,
decorticate posturing

Moderate to severe
Pupil changes,
hyperventilation,
decerebrate posturing,
seizures

Severe
Loss of respiratory
control, apnea
Progression of S/S of Increasing ICP

Severe
Respiratory arrest
Flaccidity
Ischemic response

Severe
Brain death
No spontaneous
respirations/3 minutes
Fixed pupils
Flat EEG
Ischemic Response “Cushing’s Reflex”

Increased blood pressure

Wide pulse pressure

Decreased heart rate

Loss of respirations
Assessment of Brain Function

Level of Consciousness: ABCs

Manifestations of increased ICP


Glasgow Coma Scale




headache, vomiting, pupil reactivity
Eye Opening
Best Motor Response
Verbal Response
CT scan
General Therapy for Increased ICP

Elevate HOB

Diuretics

Sedation

Hyperventilation

Decompression
Classification of Head Injury

Concussion

Contusion

Brainstem Contusion

Hemorrhage
* Epidural
* Subdural
- acute
- subacute/chronic
Intracranial Bleeds
epidural
bleed
skull
dura
arachnoid
subarachnoid
bleed
subdural
bleed
CVA: Stroke

Thrombotic


Embolic


atherosclerosis, assess carotids > age 50
atrial fibrillation, valvular disease, hypercoagulable states
Hemorrhagic


structural anomalies
hypertension
Stages of Thrombotic Stroke

Transient ischemic attacks (TIAs)

Stroke in evolution

Completed stroke
Manifestations of Stroke

Acute




focal neurological signs
may rapidly change (evolve)
depends greatly on area of brain damage
Transient Ischemic Attack (TIA)


signs and symptoms resolve quickly
no permanent loss of function
Stroke: Ischemic vs Hemorrhagic?

TIA: give ASA refer for carotid assessment

Stroke: Get CT scan immediately

Ischemic: evaluate for tPA (within 3 hours)


embolic and thrombotic
Hemorrhagic: Neurosurgical consult
Chronic Manifestations of Stroke

Contralateral hemiplegia

Ptosis

Homonymous hemianopsia

Neglect

Aphasia

Loss of bowel and bladder control

Emotional Instability
Homonymous Hemianopsia
left visual
field
right visual
field
area of stroke
damage
left visual field blindness
General Therapy for CVA

Get to a Brain Trauma Center

Prevention

Manage high blood pressure

Anticoagulation

Rehabilitation
Alzheimer Disease

Dementia (deterioration of mentation)



about 70% Alzheimer type
others are multi-infarct type (vascular)
Manifestations (JAMICO)




judgment
affect
Memory
Intellect
-confusion
-orientation
Pathology of Alzheimer Disease

Genetics VS Environment



Apo-E gene
toxins, viruses, aluminum
Pathological Findings (at autopsy)



amyloid plaques
neurofibrillary tangles
cerebral atrophy and large ventricles
Alzheimer Disease

Diagnosis of Exclusion


MRI


rule out other, potentially treatable causes
brain atrophy, enlarged ventricles
Poor mental function

Mini Mental State Exam
Seizures

Partial

Generalized
Simple (no LOC)
Absence (Petit Mal)
Complex ( LOC)
Secondarily generalized
Tonic-Clonic (Grand Mal)
Upper vs Lower Motorneuron
UMN
LMN
Reflexes
Increased
Decreased
Atrophy
No
Yes
Muscle tone
Spastic
Flaccid
Fasciculations
No
Yes
Upper Motor Neuron Disorders

Stroke/Head Injury

Cerebral Palsy

Huntington’s Chorea

Parkinson’s Disease
Localization of Motor Dysfunction

Reflexes



Deep tendon reflexes (cord reflexes)
Babinski (corticospinal tract)
Strength



focal vs general
ipsilateral vs contralateral
spasticity vs flaccidity
Parkinson Disease

Etiology


unknown, possibly neurotoxin
– some suspect pesticide exposure
– MPTP cases of Parkinson-like syndrome
Pathogenesis



Low dopamine level in basal ganglia
Excessive action of acetylcholine
Disease process is progressive
Manifestations of Parkinson Disease

Classic Triad (unilateral --> bilateral)




Akinesia
Rigidity
Resting tremor
Associated Manifestations



Propulsive gait
Masklike face
Drooling
- Poor speech quality
- 30-50% have dementia
Features of Parkinson disease
Management of Parkinson Disease

Drug Therapy is controversial

Restore Dopamine / Ach balance





MAOI (selegiline)
Amantadine (Symmetrel)
Levodopa, carbidopa (Sinemet)
anticholinergics (Cogentin, Artane)
Surgical Techniques

adrenal medulla tissue transplants
Brainstem and Spinal Cord Disorders

Multiple Sclerosis

Poliomyelitis

Spinal Cord Injury
Multiple Sclerosis

Etiology


Autoimmune attack on CNS myelin
Pathogenesis



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Immune injury to myelinated neurons
Sclerotic plaques noted on MRI
Demyelination disturbs neuron conduction
Extremely variable course and presentation
Presentation of MS

Usually relapsing remitting pattern


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paresthesias
gait disturbance
leg weakness
vision loss (optic neuritis)
double vision
arm weakness
vertigo
Diagnosis and Treatment

Suspect with episodic neurologic deficits in
20-40 age group especially Northern
European

MRI lesion is diagnostic

Treatment: symptoms


Beta interferon may decrease frequency of
attacks
Immune suppression
Transection of Spinal Cord

Spinal Shock (lasts 2-8 weeks)


loss of spinal cord reflexes below injury
– flaccidity
– decreased vascular tone - hypotension
– atony of bowel and bladder
Autonomic Dysreflexia

reflex activation of sympathetic neurons
below level of injury
Autonomic Dysreflexia
stimulus
(full bladder)
Reflex vasoconstriction
below level of injury
Increased blood
pressure
Can’t get signal
to vessels
below injury
hypertension
x
Baroreceptor Response
vasodilate above SCI
bradycardia
Q: What Pattern of Sensory-Motor
Impairment Would Occur?
transection of
lateral cord
Contralateral
motor?
sensory?
Ipsilateral
motor?
sensory?
Lower Motor Neuron Disorders

Bell’s Palsy
Guillian Barre’ Syndrome
Guillain Barre’ Syndrome

Most common cause of acute flaccid
paralysis

Presentation: Back leg pain progressing to
weakness




decreased DTRs
Hx viral infection esp. mono preceding
decreased nerve conduction velocity
Hospitalize, plasmapheresis, IgG
Disorder of Neuromuscular Junction

Myasthenia Gravis


80%-90% have anti-receptor antibodies
75% have abnormal thymus
YY Y
Myasthenia Gravis

Presentation: NM fatigue which worsens with
activity: eye droop, diplopia, head droop, jaw
dropping

No loss of reflexes, no change in sensation

Respond to edrophonium (fast acting
anticholinesterase)
Muscle Disorders

Muscular Dystrophy
Disorders of Hearing

Conductive hearing loss



otosclerosis
otitis media
Sensorineural hearing loss


Presbycusis
Menière Disease
Disorders of Vision

Errors of Refraction

myopia, hyperopia, presbyopia

Cataract

Retinal detachment

Glaucoma

increased intra-ocular pressure
Open Angle Glaucoma
fluid
Increased
anterior
chamber
IOP
clogged canal of Schlemm
Closed Angle Glaucoma
fluid
Increased
anterior
chamber
IOP
plugged canal of Schlemm
when pupil dilates (acute)
Open and Closed Angle Glaucoma
Sensory dermatomes
Pain Transmission

Gate Theory
Uses the analogy of a gate to describe how
impulses from damaged tissues are sensed
in the brain.
Pain Transmission, con’t.

Tissue injury stimulates the release of:
*
*
*
*
*
Bradykinin
Histamine
Potassium
Prostaglandins
Serotonin
Pain Transmission, con’t.

“A” Fibers
*
*
*
*
myelin sheath
large fiber size
conduction is fast
inhibits pain
transmission
* Sharp & welllocalized

“C” Fibers
*
*
*
*
no myelin sheath
small fiber size
conduction is slow
facilitates pain
transmission
* dull & non-localized
Pain Transmission, con’t.
Types of pain are related to the proportion of
“A” to “C” fibers
in the damaged tissue.
Pain Transmission, con’t.
These two pain fibers enter
the spinal cord at the dorsal
horn and travel up to the
brain.
This is the location of the
GATE
Pain Transmission, con’t.
The gates regulate the flow of sensory
impulses to the brain!
If the gate is closed – no impulses get
through. Therefore no impulses are
transmitted to the higher centers in the
brain so there is no perception of PAIN!
Pain Transmission, con’t.
It’s the large, activated “A” fibers that
closes the gate
and this will inhibit transmission to the
brain and limits perception of
PAIN!
Pain Transmission, con’t.
It’s the small, activated “C” fibers that
opens the gate
and this will allows transmission to the
brain and causes perception of
PAIN!
Pain Transmission, con’t.

Nerve fibers from the brain innervate the GATE
and allow the brain some control over the
GATE….in that the brain can:
* evaluate the pain
* identify the type of pain
* localize the pain

This also allows the brain to control the GATE
before the gate is open.
Pain Transmission, con’t.
Along with the “A” and “C” fibers, there are
specialized cells that control the GATE –
these are the “T” cells, which have a
threshold…meaning that impulses must
overcome the threshold in order to be
sent to the brain.
Pain Transmission, con’t.

Body produces endogenous
neurotransmitters:
* Enkephalins & Endorphins

They are produced by the body to:
(1) fight pain
(2) bind to opioid receptors
(3) inhibit transmission of pain
impulses by closing the GATE.
Measures to  Close the GATE

Rubbing the painful area
(this inhibits the large “A” sensory fibers

Give the opiates to close the GATE
(this will reduce recognition of pain)
Hang in there –
just one more
week!!