neurological disorders cerebral hemispheres brainstem

Neurological Disorders

Neurological Disorders

Cerebral hemispheresBrainstem & Cerebellum

Spinal CordSpinal and Cranial

Structural Organization

Nervous System Function

Brain: Central Processing Unit

Sensory Inputsafferent

efferent

Secretion Movement

Sensory Tracts

dorsalanterolateral

Dorsal column ipsilateral until

medulla, then crosses

sensation is well localized

touch, vibration, pressure,

Major Sensory Tracts

Anterolateral (Spinothalamic) crosses

immediately in the cord

sensation is poorly localized

itch, pain, temp

Medial Tracts some tracts

cross at medulla, some don’t

innervates axial muscles

balance, gross motor

Major Motor Tracts

Lateral Corticospinal crosses at medulla innervates distal

muscles fine motor control

How Do Neurons Communicate?

dendrite

axon

axonterminal

synapse

postsynapticneuron

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)

Neurotransmitter Classes

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

Ischemia

ATP deficiencyRelease ofglutamate

“excitotoxin”

Na+, Ca++ in cell

Activation ofphospholipases

mitochondriadysfunction

free radicalsprostaglandinsthromboxanes

cell damagevasospasmplatelet plug

Pathophysiology of Secondary Injury

Compensation for Increased ICP

Brain Swelling

CSF shunted to spinal cord

CSF in brain ventricles

ICP

ICPHyperventilation

PaCO2

Cerebral vasoconstriction

Blood in brain

ICP

Progression of S/S of Increasing ICP

Mild to moderate

Moderate to severe

Severe

Headache, LOC, projectile vomiting, localized pain, decorticate posturing

Pupil changes, hyperventilation, decerebrate posturing, seizures

Loss of respiratory control, apnea

Progression of S/S of Increasing ICP

Severe

Severe

Respiratory arrestFlaccidityIschemic response

Brain deathNo spontaneous respirations/3 minutesFixed pupilsFlat 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 headache, vomiting, pupil reactivity

Glasgow Coma Scale 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

skull

dura

arachnoid

epiduralbleed

subduralbleed

subarachnoidbleed

CVA: Stroke

Thrombotic atherosclerosis, assess carotids > age 50

Embolic atrial fibrillation, valvular disease, hyper-

coagulable 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

area of strokedamage

right visualfield

left visualfield

left visual field blindness

Homonymous Hemianopsia

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 -confusion affect -orientation Memory Intellect

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 rule out other, potentially treatable causes

MRI brain atrophy, enlarged ventricles

Poor mental function Mini Mental State Exam

Seizures

Partial

Simple (no LOC)

Complex ( LOC) Secondarily generalized

Generalized

Absence (Petit Mal)

Tonic-Clonic (Grand Mal)

Upper vs Lower Motorneuron

UMN

Reflexes Increased Decreased

Atrophy No Yes

Muscle tone Spastic Flaccid

Fasciculations No Yes

LMN

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 - Poor speech quality Masklike face - 30-50% have dementia Drooling

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 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 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 vasoconstrictionbelow level of injury

Increased bloodpressure

Baroreceptor Response

bradycardiavasodilate above SCI

xCan’t get signal to vesselsbelow injury

hypertension

transection of lateral cord

Contralateralmotor?sensory?

Ipsilateralmotor?sensory?

Q: What Pattern of Sensory-Motor Impairment Would Occur?

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

YYY

Disorder of Neuromuscular Junction

Myasthenia Gravis 80%-90% have anti-receptor antibodies 75% have abnormal thymus

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

clogged canal of Schlemm

IncreasedanteriorchamberIOP

Closed Angle Glaucoma

fluid

plugged canal of Schlemm when pupil dilates (acute)

IncreasedanteriorchamberIOP

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


“A” Fibers

* myelin sheath* large fiber size* conduction is fast* inhibits pain transmission* Sharp & well- localized

“C” Fibers

* no myelin sheath* small fiber size* conduction is slow* facilitates pain transmission* dull & non-localized


Types of pain are related to the proportion of

“A” to “C” fibers

in the damaged tissue.


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


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!


It’s the large, activated “A” fibers that

closes the gate

and this will inhibit transmission to the brain and limits perception of

PAIN!


It’s the small, activated “C” fibers that

opens the gate

and this will allows transmission to the brain and causes perception of

PAIN!


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.


Along with the “A” and “C” fibers, there arespecialized 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.


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!!

neurological disorders cerebral hemispheres brainstem

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