Chapter 14: Nervous System Disorders Study Guide

Overview of the Nervous System Components

Central Nervous System (CNS): - Comprised of the Brain and the Spinal cord.
Peripheral Nervous System (PNS): - Cranial nerves. - Spinal nerves. - Peripheral nerves. - Ganglia: Clusters of neuron cell bodies located outside the CNS. - Sensory receptors: Located in various tissues, such as the skin, to detect stimuli. - Enteric plexuses: Specialized nerve networks located in the small intestine used for digestive control.

The Meninges and Spaces

Structural Layers (External to Internal): - Skin: The outermost protective layer. - Muscle: Tissue underlying the skin. - Periosteum: Membrane covering the outer surface of the bone. - Bone: The skull provide rigid protection. - Dura mater: The tough, outermost meningeal layer. - Arachnoid mater: The middle web-like meningeal layer. - Pia mater: The delicate, innermost layer adhering directly to the brain and spinal cord surface.
Anatomical Spaces: - Epidural space: Located between the bone and the dura mater. - Subdural space: Located between the dura mater and the arachnoid mater. - Subarachnoid space: Located between the arachnoid and pia mater; contains cerebrospinal fluid (CSF).

Characteristics of Normal Cerebrospinal Fluid (CSF)

Appearance: Clear and colorless.
Pressure: Ranges from $9-14\,mmHg$ or $150\,mm\,H_2O$ .
Cell Counts: - Red blood cells: None. - White blood cells: Occasional.
Chemical Composition: - Protein: $15-45\,mg/dL$ . - Glucose: $45-75\,mg/dL$ . - Sodium: $140\,mEq/L$ . - Potassium: $3\,mEq/L$ .
Physical Properties: - Specific gravity: $1.007$ . - pH: $7.32-7.35$ .
Quantity and Production: - Volume in system at one time: $125-150\,mL$ . - Volume formed in 24 hours: $500-800\,mL$ .

Brain Protection and Barriers

Blood-brain barrier (BBB): - Located at the level of capillaries in the brain. - Functions: Limits the passage of materials into the brain; controls the balance of electrolytes, glucose, and proteins. - Permeability: Lipid-soluble substances pass through easily. - Developmental Note: This barrier is poorly developed in neonates.
Blood-CSF barrier: - Located at the choroid plexus. - Function: Controls the specific constituents of the cerebrospinal fluid.

Functional Areas of the Brain

Frontal Lobe: - Motor Cortex: Controls voluntary movement (includes areas for the foot, leg, trunk, arm, hand, and face). - Premotor Cortex: Responsible for skilled movements. - Broca’s Speech Area: Specifically manages the motor aspects of speech. - Intellect and Personality: Executive functions and character traits are rooted here.
Parietal Lobe: - Sensory Cortex: Processes physical sensations.
Occipital Lobe: - Visual Area: Primary processing of visual information. - Visual Association Area: Interpretation of visual stimuli.
Temporal Lobe: - Auditory Area: Processes sound. - Wernicke’s Area: Responsible for the comprehension of speech. - Memory: Storage and retrieval of information.
Brainstem and Lower Brain: - Cerebellum: Coordinates balance, equilibrium, and skeletal muscle coordination. - Pons and Medulla: Contain vital centers (respiratory/cardiovascular) and the Reticular Activating System (RAS).

The Autonomic Nervous System (ANS)

Sympathetic Nervous System: - Pathway: Impulse travels from the spinal cord to a ganglion via a preganglionic nerve, then through a postganglionic nerve to the receptor. - Neurotransmitters: Uses Acetylcholine at the ganglion and Norepinephrine at the target receptor.
Parasympathetic Nervous System: - Pathway: Impulse travels from the brain or spinal cord via a preganglionic nerve, through a ganglion, and via a postganglionic nerve to the receptor. - Neurotransmitters: Uses Acetylcholine at both the ganglion and the target receptor.

Local (Focal) Effects and Hemispheric Damage

Local/Focal Effects: These are signs related to the specific area of damage in the brain or spinal cord. - Example: Paresis or paralysis of the right arm results from damage to a specific section of the left frontal lobe. - Expanding Lesions: Caused by growing tumors or hemorrhages. As the lesion grows, additional impairment occurs as adjacent brain areas become involved.
Left Hemisphere Damage: - Loss of logical thinking ability and analytical skills. - Deficits in intellectual and communication skills.
Right Hemisphere Damage: - Impairs the appreciation of music and art. - Causes behavioral problems. - Deficits in spatial orientation and recognition of relationships. - Self-care deficits are common.

Seizure Disorders

Definition: Caused by spontaneous, excessive discharge of neurons in the brain.
Etiology: inflammation, hypoxia, or bleeding in the brain.
General Classifications: - Focal Seizures: Related to a particular site of irritation; may eventually become generalized. Often manifested by involuntary repetitive movements or an abnormal sensation known as an "aura." - Generalized Seizures: - Absence seizures (petit mal): Brief lapses in consciousness. - Tonic-clonic (grand mal): Characterized by muscle rigidity (tonic) followed by jerking (clonic). - Myoclonic: Sudden, brief muscle jerks. - Partial Seizures: - Simple partial. - Complex partial (psychomotor). - Status Epilepticus: Continuous seizures without recovery of consciousness. This leads to increased metabolism of glucose and oxygen and may be life-threatening.
Symptom Progression for Generalized Seizures: - Prodromal signs: Occur hours before the event. - Aura: Precedes loss of consciousness. - Tonic Phase: Strong muscle contraction and a "cry." - Clonic Phase: Rhythmic contractions that gradually subside. - Postictal Period: Post-seizure phase where the person is confused, fatigued, has aching muscles, and falls into a deep sleep.

Transient Ischemic Attacks (TIAs)

Characteristics: These may occur singly or in a series and result from temporary localized reduction of blood flow in the brain.
Pathophysiology Causes: - Partial occlusion of an artery (Atherosclerosis). - Small embolus. - Vascular spasm. - Local loss of autoregulation.
Signs and Symptoms: - Intermittent short episodes of impaired function (e.g., muscle weakness in arm/leg). - Visual disturbances. - Numbness and paresthesia in the face. - Transient aphasia or confusion. - Note: Repeated TIAs may be a warning sign for full obstruction related to atherosclerosis.

Cerebrovascular Accidents (CVAs)

Definition: Also known as a stroke; an infarction of brain tissue resulting from lack of blood/oxygen.
Causal Mechanisms: - Occlusion of a cerebral blood vessel: (Ischemic stroke). - Rupture of cerebral vessel: (Hemorrhagic stroke).
Cellular Impact: Five minutes of ischemia causes irreversible nerve cell damage. A central area of necrosis develops where all function is lost, surrounded by a zone of inflammation that may regain function after healing.
Detailed Types of CVAs: - Thrombus: Caused by atherosclerosis in a cerebral artery. It has a gradual onset (often at rest), minimal increased intracranial pressure (ICP), and localized effects that may be less permanent if collateral circulation exists. - Embolus: Caused by atherosclerosis in carotid arteries or systemic sources like the heart. It has a sudden onset and localized effects unless multiple emboli are present. - Hemorrhage: Caused by hypertension-related arteriosclerosis. It has a sudden onset (often occurs with activity), presents with high ICP, and has widespread, severe, and often fatal effects.
Etiology/Risk Factors: - Diabetes, hypertension, systemic lupus erythematosus (SLE), atherosclerosis. - Age, history of TIAs, heart disease, smoking, sedentary lifestyle. - Obstructive sleep apnea. - Combination of oral contraceptives and cigarette smoking. - Congenital malformation of blood vessels.
Signs and Symptoms: - Lack of voluntary movement/sensation on the opposite side of the body. - Initially flaccid paralysis; spastic paralysis develops weeks later. - Diagnostic Tool: NIH Stroke Scale (NIHSS) developed by the National Institutes of Health.
Treatment: - Clot-busting agents (for ischemic types). - Surgical intervention. - Glucocorticoids to reduce inflammation. - Supportive treatment (Physio, Occupational, and Speech therapy). - Rehabilitation should begin immediately.

Meningitis

Description: An infection, usually of bacterial origin, involving the meninges. Early diagnosis is essential.
Pathophysiology: - Microorganisms reach the brain via blood, nearby tissue, or direct access. - Infection spreads rapidly through the meninges; inflammatory response leads to increased ICP. - Exudate is present in the CSF. - Blood vessels on the brain surface appear dilated.
Etiology by Age Group: - Neonates: $Escherichia\,coli$ . Often linked to neural tube defects, premature rupture of amniotic membranes, or difficult delivery. - Young Children: $Haemophilus\,influenzae$ . More common in autumn or winter. - Children and Young Adults: $Neisseria\,meningitides$ (meningococcus). - Older Adults: $Streptococcus\,pneumoniae$ .
Signs and Symptoms: - Sudden onset, severe headache, back pain, and fever/chills. - Photophobia (sensitivity to light). - Nuchal rigidity: Stiff neck. - Kernig sign: Resistance to leg extension when the hip is flexed. - Brudzinski sign: Neck flexion causes hip/knee flexion. - Progression to stupor or seizures.
Diagnostics and Treatment: - ** Lumbar Puncture:** Examination of CSF to identify the organism. - Therapy: Aggressive antimicrobial therapy and glucocorticoids.

Head Injuries

Concussion (Minimal Brain Trauma): - Reversible interference with brain function caused by sudden excessive movement (mild blow or whiplash). - Symptoms: Amnesia and headaches. Recovery usually within $24\,hours$ .
Contusion: - Bruising of brain tissue, rupture of small blood vessels, and edema caused by a blunt blow. Possible residual damage.
Injury Mechanics: - Closed Head Injury: Direct injury involves the initial impact; Contrecoup injury occurs when the brain rebounds and hits the opposite side of the skull. - Open Head Injury: Depressed fracture where bone fragments penetrate the brain, causing bleeding and edema.

Multiple Sclerosis (MS)

Definition: Progressive demyelination of neurons in the brain, spinal cord, and cranial nerves.
Pathophysiology: - Loss of myelin interferes with impulse conduction. - Earliest lesions: Inflammatory response and myelin loss in white matter. - Plaques: Larger areas of inflammation and demyelination that become visible on MRI, commonly near lateral ventricles, brainstem, and optic nerve. - Neural Regeneration: Inflammation may subside initially, allowing function to return temporarily, but recurrent attacks lead to irreversible degeneration.
Etiology: Onset usually between $20-40\,years$ of age. Possible autoimmune, nutritional, genetic, or environmental causes.
Signs and Symptoms: - Blurred vision, diplopia (double vision), scotoma (blind spot) due to optic nerve involvement. - Dysarthria (speech difficulty). - Paresthesia, numbness, burning, tingling. - Progressive weakness/paralysis, loss of coordination (ataxia/tremor), and chronic fatigue. - Bladder, bowel, and sexual dysfunction.

Parkinson’s Disease

Definition: Progressive degenerative disorder of the extrapyramidal motor system.
Pathophysiology: Degeneration in the basal nuclei and an imbalance between excitation and inhibition, leading to excess stimulation.
Etiology: - Primary: Idiopathic; usually develops after age $60$ . - Secondary: Caused by encephalitis, trauma (sports), vascular disease, or drugs (phenothiazine tranquilizers).
Clinical Manifestations: - Early signs: Fatigue, muscle weakness, decreased flexibility, pill-rolling tremors of hands at rest. - Motor signs: Muscle rigidity, difficulty initiating movement, slow movements (bradykinesia). - Posture and Gait: Stooped posture, leaning forward, propulsive/shuffling gait. - Other systems: Mask-like facial expression, reduced blinking, low-inflection voice, chewing/swallowing difficulties, and drooling. - Autonomic dysfunction: Urinary retention, constipation, and orthostatic hypotension.
Treatment: Dopamine replacement therapy (Levodopa), Monoamine oxidase B inhibitors, and anticholinergic drugs.

Amyotrophic Lateral Sclerosis (ALS)

Definition: Also known as Lou Gehrig’s disease; a progressive degenerative disease affecting motor neurons.
Affected Areas: - Upper Motor Neurons (Cerebral Cortex): Damage leads to spastic paralysis and hyperreflexia. - Lower Motor Neurons (Brainstem/Spinal Cord): Damage leads to flaccid paralysis, decreased muscle tone, and loss of reflexes.
Key Features: Cognition remains unimpaired. Death typically occurs due to respiratory failure.
Treatment: Riluzole (Rilutek) to slow neuron damage; stem cell therapy is under investigation.

Dementia and Alzheimer’s Disease

Dementia (General): Progressive chronic disease characterized by decreased cortical function, impaired memory, thinking, and personality changes.
Alzheimer’s Disease (AD): - Pathology: Progressive cortical atrophy, development of neurofibrillary tangles and plaques, and a deficit in Acetylcholine (ACh) due to neuron loss. - Symptoms (over 10–20 years): - Behavioral: Irritability, hostility, mood swings. - Cognitive: Gradual loss of memory, lack of concentration, poor judgment, decline in language. - Physical/Functional: Incontinence, inability to recognize family, and loss of environmental awareness.