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HCR240-Chapter34ChronicandDegenerativeNeurologicalDisorders.pptx

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Chapter 34

Chronic and Degenerative Neurological Disorders

Basic Neurological Concepts

Central nervous system (CNS)

Brain and spinal cord

Peripheral nervous system (PNS)

Somatic nerves (motor and sensory)

Autonomic nervous system (ANS)

Neurons

Conduct electrical signals

Glial cells

Support cells

Neurotransmitters

Released at synapse

Each neuron produces one type of neurotransmitter

Acetylcholine

CNS, PNS, ANS

Excitatory or inhibitory

Serotonin

5-hydropxytryptamine

CNS: well-being

Neurotransmitters (continued)

Dopamine

CNS

Many functions: behavior, movement, memory

Gamma amino butyric acid (GABA)

CNS, inhibitory

Norepinephrine

Excitatory stress hormone

Glutamate

Excitatory signal in CNS

Nerve Conduction

Movement of ions

Depolarization

Sodium influx

Repolarization

Potassium efflux

Resting membrane potential

Refractory period

Brain

Cerebral cortex

Higher order brain function, separated into lobes

Cerebellum

Coordination, balance, posture

Ataxia: gait disturbance and imbalance

Diencephalon

Consists of hypothalamus and thalamus

Major Components of Brain

Brainstem

Midbrain

Vision, hearing, movement

Pons

Consciousness and sleep

Medulla oblongata

Vital body functions

Basal ganglia

Portion of the midbrain, modulates voluntary motor function

Substantia nigra

Portion of basal ganglia, synthesizes dopamine

Myelin

Protective sheath around axon of some neurons

Insulator

Myelin sheath contains lipids

Referred to as “white matter”

Helps conduct electrical signal more quickly

Some disorders cause degeneration of myelin

Multiple sclerosis, amyotrophic lateral sclerosis

Regrowth may be possible for some time

Ion Channel Disorders

AKA: channelopathies

Mutation in gene or autoimmune attack

Example: epilepsy

Disrupted channel activation leading to repetitive synchronous firing of neuronal action potentials

Epilepsy

Chronic neurological disorder with recurrent seizures

Seizure

Sudden, abnormal, disorderly discharge of neurons within the brain

Manifestations depend on area affected

Traditional diagnosis

2 unprovoked seizures at least 24 hours apart

Epileptogenesis

Transformation of normal neuronal region into hyperexcitable area

Seizure Types

Focal: localized within 1 cerebral hemisphere

Initiation phase

High frequency action potentials and hyper synchronization

Can see spike on EEG

Generalized: involve both hemispheres

2017 International League Against Epilepsy (ILAE): 3 major categories of seizures

Generalized onset

Focal onset

Unknown onset

Seizures

Cause motor, nonmotor or both symptoms

Clonic

Sustained rhythmical jerking

Atonic

Weak or limp muscles

Myoclonus

Muscle twitching

Nonmotor symptom

“Absence seizures” (staring spells with no movement)

Seizures (continued)

Aura

Sensation before a seizure

Ictal period

Time of seizure

Postictal

After seizure complete

Person may be tired, confused, nauseated, may have amnesia

Interictal

If multiple seizures occur in short time, the time between seizures

Seizure Etiology

Head trauma

Most common

Stroke

Elderly

Brain neoplasms

Congenital malformation

Degenerative brain disorders

i.e., Alzheimer’s disease

Environmental stimuli

Blinking lights

Genetic predisposition

Head trauma

Infections

Metabolic disturbances

Hypoglycemia

Hyponatremia

Respiratory alkalosis

Perinatal injury

Hypoxia

Withdrawal from alcohol or sedative-hypnotic drugs

Diagnostic Tests

Complete blood count (CBC)

Serum chemistry

Brain imaging studies

Magnetic resonance imaging (MRI)

Computed tomography (CT) scan

EEG

Sleep deprivation will increase sensitivity

Emergency Seizure Care

During a seizure, protect the patient from injury

Move objects out of the way

Do not physically restrain

Do not put anything in his or her mouth

After seizure has ended, place the patient on his or her left side and turn the head

Any emesis or oral secretions will drain out of the mouth and will not be inhaled

Epilepsy Treatment

Antiepileptic agents

Modify ion channels or neurotransmitters in brain

Phenytoin, valproic acid, carbamazepine, etc.

Decrease seizure risk while limiting adverse side effects of medications

Headaches

Primary headaches

Arise independent of any other medical illness or traumatic cause

Tension-type, migraine, and trigeminal autonomic cephalgia

Secondary headaches

Caused by another primary condition

Head injury, vascular problems, medication side effects, sinus disease, and tumors

Tension Type Headache (TTH)

Most common type of primary headache

Infrequent, frequent, and chronic

Bilateral pain with mild to moderate pressure

Does not worsen with physical activity

No associated nausea or vomiting

Increased cervical and pericranial muscle activity

Tension Type Headache (TTH) (continued)

Diagnosis

Clinical finding

Treatment

Pain relievers

Relaxation therapy

SSRI’s (for chronic forms)

Migraine Headache

Periodic, throbbing headaches

Altered perceptions, nausea, and severe pain

Photophobia and phonophobia

Usually worsens with movements

Aura may precede headache

75% of migraine sufferers are women

Migraine Headache (continued)

Prodrome

Neural hyperexcitability

Aura

Cortical spreading depression occurs

Pain

Trigeminovascular complex activation

Postdrome

Sensitization of the trigeminovascular complex persists

Most migraines have common pattern of presentation in an individual

Patients may keep migraine diary, help identify triggers

Migraine Pathophysiology

Serotonin decrease and calcitonin gene-related peptide (CRGP) increase thought to play a role

CRGP is a vasodilator

Dopamine may also play a role

Triggers

Stress

Hormone shifts

Excessive exercise

Lack of sleep

Fatigue

Hypoglycemia

Certain foods

Migraine Treatment

NSAID’s

Serotonin receptor agonists (triptans)

Dopamine receptor antagonists

Preventive, prophylactic therapy may be considered in chronic migraine sufferers

Clostridium botulinum (Botox®) injections may help

Trigeminal Autonomic Cephalgia (TAC)

Excruciating, unilateral headache

Cranial parasympathetic features

Most common in males age 25 to 50 years

Types

Cluster headache

Paroxysmal hemicrania

Vasodilation causes pain and autonomic features

Trigeminovascular system is activated

Trigeminal Autonomic Cephalgia (TAC) (continued)

Unilateral orbital, supraorbital, or temporal

Last 15 to 180 minutes

Occur several times a day

“Blood shot” eyes, tearing of eyes, rhinorrhea, pupil constriction, eyelid edema

Person struggles to sit quietly

Diagnosis

Clinical presentation

Treatment

100% oxygen inhalation or subcutaneous sumatriptan

Sinus Headache

Caused by sinus infection

Fever and rhinorrhea may be present

Pain worsens when the patient leans over

Facial areas over frontal and maxillary sinuses may be tender

Transillumination of the sinuses may show nontransparency

Treatment with antibiotics (if infection present) and nasal decongestants

Brain Tumor Headache

50% of those with brain tumor will experience headache

Headache is dull and constant, may throb

Usually bifrontal, with worse pain on the same side as the tumor

Generalized head pain may occur with increased intracranial pressure

Papilledema and cranial nerve abnormalities may be present

Brain Tumor Signs

Abnormal neurological examination

Change in prior headache patterns

Worsening of headache with a change in body position

Any maneuver that raises intrathoracic pressure or intracranial pressure

Worsening headaches at night that awaken the patient from sleep

Parkinson’s Disease

Unknown etiology

Men and women equally affected

Progressive loss of dopamine-producing cells in the substantia nigra

Movements, such as posture, standing, walking, and writing affected

Acetylcholine stimulates muscle movement, while dopamine has an inhibitory effect

Dopamine depletion imbalance causes unopposed acetylcholine (tremors, uncoordinated movements)

Parkinson’s Disease (continued_1)

Also accumulation of alpha-synuclein, abnormal protein found in structures called Lewy bodies in the brainstem, spinal cord, and regions of the cortex

Accumulation associated with neurodegeneration

Can also affect ANS, causing nonmotor symptoms

Parkinson’s Disease (continued_2)

Symptoms initially begin unilaterally, but progress to both sides

Classic triad

Bradykinesia (also episodes of akinesia)

Resting tremor (“pill-rolling”)

Muscle rigidity (cogwheel, ratchet movement)

Additional symptoms

Postural instability

Nonmotor, neuropsychiatric

Diagnosis of Parkinson’s Disease

TRAP

Tremor at rest

Rigidity

Akinesia (or bradykinesia)

Postural/gait instability

No laboratory tests

Treatment of Parkinson’s Disease

Levodopa (L-dopa)

Metabolic precursor of dopamine

Carbidopa in combination

Inhibits peripheral metabolism of levodopa

Diminishing returns with long-term levodopa usage

Surgical procedures

Multiple Sclerosis (MS)

Chronic demyelinating disorder

Affects brain, spinal cord, and optic nerves

Characterized by remissions and exacerbations

Myelin damage heals during remission

Unknown etiology

Autoimmune component thought to be involved

Multiple Sclerosis (MS) (continued_1)

Risks

Genetic predisposition, viral process, trauma, female, Northern European descent, living in cooler climates

Both sensory and motor neurons affected

T cell-mediated attack of myelin

Relapse and remission in most forms

Primary progressive MS (PPMS): No remission

Occurs in 10%–15% of individuals with MS

Multiple Sclerosis (MS) (continued_2)

Symptoms

Weakness, numbness, balance problems, blurred vision

Dysphagia, hemiparesis, paraparesis may develop

Cognitive functioning

Recent memory, abstract reasoning, attention can be affected

Affective symptoms

Depression

Multiple Sclerosis (MS) (continued_3)

Diagnosis

Lesions of demyelination

McDonald criteria

MRI evidence and patient symptoms

Blood work to rule out other conditions with neurological presentation

Lyme disease, syphilis, etc.

CSF analysis

Multiple Sclerosis (MS) (continued_4)

Treatment

Immunomodulating agents

Corticosteroids

Immunosuppressants

Guillain-Barré Syndrome (GBS)

Postinfectious disease

Acute inflammatory demyelination

Weakness varies from mild weakness to complete paralysis, including respiratory muscles

Recovery is often steady over weeks and months

Treatment

Supportive as life-threatening sequelae may develop

Immunomodulating agents

Myasthenia Gravis (MG)

Autoimmune disease

Attack of Ach receptors

Diagnosis

Ach receptor antibodies

Muscle weakness and fatigue

Commonly, the extraocular muscles often affected first; ptosis

Myasthenia Gravis (MG) (continued_1)

B-cell and T-cell mediated

Thymus may be involved in this disease

Approximately 70% of patients with MG have thymus gland hyperplasia

Presents in two ways

Ocular form: often patients first present with ocular changes

General form

Myasthenia Gravis (MG) (continued_2)

True muscle fatigue

Not a sense of tiredness

Decreased contractile force

Occurs with repetitive motions

Blinking, walking, talking, chewing

Swallowing and respiratory function may be affected

Rest improves muscle function

Myasthenia Gravis (MG) (continued_3)

Diagnosis

Edrophonium (Tensilon®) testing

Acetylcholinesterase inhibitor

Allows more Ach to remain in the synapses for a longer period of time

30–45 seconds after administration, improved muscle contraction

Serum Ach receptor antibodies

EMG

Treatment of MG

Physostigmine

Acetylcholinesterase inhibitor

Other treatments

Intravenous immune globulin

Plasmapheresis

Thymectomy may be recommended

learning guide M6

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