Week 12 (EXAM 3)

Question 1

What is the R & L hemispheres of the brain responsible for?

Answer 1

1) R: creative mind
2) L: logical mind

Question 2

What are the components of the frontal lobe? What do they control?

Answer 2

prefrontal area (left cortex): intellectual function and personality

Prefrontal association area: conscious thought

Pre motor cortex: skilled movements, muscle coordination

Motor cortex: voluntary movements

Broca area (left cortex): speech “expression” (motor speech)

Question 3

What are the components of the parietal lobe? What do they control?

Answer 3

somatosensory area: perception, sensation (touch, pain…)

Question 4

What are the components of the occipital lobe? What do they control?

Answer 4

visual cortex: vision

Question 5

What are the components of the temporal lobe? What do they control?

Answer 5

auditory cortex: hearing

Olfactory cortex: smell

Wernicke area (left cortex): comprehension of speech memory (sensory speech)

Question 6

What does the cerebellum control?

Answer 6

body balance and position, coordinated movement

Question 7

What does the medulla oblongata control?

Answer 7

1) control and coordination centers for respiration and cardiovascular activity

2) swallow reflex center, vomiting reflex, cough reflex

3) nuclei of five cranial nerves

Question 8

Which subcortical structure is the “sensory relay station”?

Answer 8

thalamus: sensory processes with 1 exception. Sensory information of Smell, it does not pass through the thalamus.

Question 9

What are the main structures of brain stem? What do they do?

Answer 9

1) midbrain
2) pons
3) medulla

A) provides innervation to head and neck by cranial nerves
B) Contains nuclei associated with important body functions:
Regulation of blood pressure
Respiration
Swallowing
Bladder control
Sleep cycle

Question 10

What are the layers of meninges?

Answer 10

1) dura mater (periosteal and meningeal layers)
2) arachnoid mater: has CSF, serves as a shock absorber, has nutrients
3) pia mater

Question 11

what is the function of the hypothalamus?

Answer 11

Hypothalamus:
Control center of the autonomic nervous system
Homeostatic regulation

The hypothalamus links the nervous system to the endocrine system via the pituitary gland.
Contains nuclei that regulates body temperature, food and water intake, sleep and wake cycle, and memory and emotional behavior

Question 12

What is an intercranial pressure issue?

Answer 12

(normal 5-15 mmHg)

Increased pressure can arise from the 4 ventricles due to increased CSF

Symptoms:
Decreasing level of consciousness
Headaches, vomiting
Increased BP, bradycardia
Visual changes
Pupillary changes
Normally no RBC in CSF (some WBC and specific number of glucose and proteins)

Cautions:
No heavy lifting
Monitor BP
Head should be elevated in bed

Question 13

Describe CNS infection

Answer 13

Meningitis & encephalitis:
Mostly viral infection, affects actual brain tissue, spreads easily in crowded conditions, pathogens reach brain via blood from inner ear.
(Bacterial more likely to have lasting effects)

VIP early detection for children especially.
Can be lyme or herpes

Signs and symptoms:
Altered mental status, headache, fever, stiff neck, light sensitivity, fever
Can spread through subarachnoid space, can be deadly (needs early detection)

Approach:
Test by spinal puncture/tap
Kernig sign: tests for meningeal irritation
Corticosteroids
Antibacterial
Antiviral

Question 14

Describe brain neoplasm

Answer 14

(All of them affect glial tissue, all need a craniotomy)
They can trigger seizures and increase inter-cranial pressure

1) olgiodendrogiloma: 3% of adult brain neoplasms, slow growing, can be malignant

2) astrocytoma low grade: 10% of adult brain neoplasm (common in children), slow growing, is a malignancy, structure and function of glial cells is affected

3) glioblastoma multiforme: 50% of adults with primary brain neoplasm, poor survival rate (most severe out of the 3), usually occurs for those 50 yo or older, malignant

Treatment:
Chemotherapy
Debunking of tumor (craniotomy)
Radiation

Question 15

Describe Cerebral Vascular Accident

Answer 15

(#1 disabler of neurogenic disorders)
(Aka heart attack of the brain, vascular disease)

2 types: ischemic stroke and hemorrhagic stroke (most deadly)

1) Ischemic (85%):
(TPA for treatment within 6 hours or less) (TIA, thrombotic, embolic, anticoagulant) (it can have warning signs of a stroke but last less than 24 h)
A) atherosclerotic CV disease (hypoperfusion, arteriogenic embolism)
B) penetrating artery disease (lacunae strokes)
C) cardiogenic embolsim
D) cryptogenic stroke

2) hemorrhagic (15%):
A) microvasc disease
B) HTN
C) microaneurysms
D) surgery (craniotomy)
E) hemipare sis (flaccid paralysis on one side -> spasticity)

Signs & symptoms:
BE FAST
B: balance, E: eyes (vision loss), F: face (uneven), A: arms (weakness in one arm), S: speech (slurred or confused), T: time (call 911)

Risk factors:
50 or older, black or female, coronary artery disease, hypertension, Afib, patent foramen ovals, diabetes, diet & smoke

Question 16

Describe cerebral circulation territories

Answer 16

1) vertebral arteries come up and supply posterior brain

2) internal carotids branch to supply anterior and medial brain tissue

Question 17

Describe physiology of ischemic CVA

Answer 17

Permissive HTN (hypertension): To allow for maximal perfusion of the pneumbra, we typically allow patients in the first few days post stroke to run high on BP (220/120mmHg) if they have not received tPA (180/105 if received tPA). Watch the orders for parameters. (Not as high if pt had tPA)

Precautions: Often on blood thinners so bruise/bleed easily—fall risk precautions.

Extension of stroke (symptoms expand). Hemorrhagic conversion=>brain bleed after ischemic CVA.

Pt needs an anticoagulant

Secondary issue: at the surrounding area (penumbra) due to inflammatory process triggering neurotoxicity

Question 18

Describe traumatic brain injury

Answer 18

(coup - contra coup injury) impact and rebound of skull

Typical pt: young got in an accident, children learning to walk, women over 50 yo form falls

Primary damage (trauma):
1) skull fracture (tissue damage and bleeding)
2) contusion (edema and minor bleeding)
3) brain motion (rotation and shearing of brain leading to damage and bleeding)

Secondary damage:
bleeding, inflammation and edema, hematoma, possible infection

Both lead to:
1) increased intracranial pressure
2) ischemia and necrosis
3) loss of vital functions like respiratory and cardiovascular control

Question 19

Describe the Glasgow coma scale

Answer 19

Tool assessing brain injury

mild = 13-15
Mod = 9-12
Sever = <9

<13 is a brain injury not a concussion

Checks eye opening, verbal, and motor responses

Question 20

Describe diffuse axonal injury

Answer 20

Anterior and posterior portions of corpus callosum are stretched and damaged

Brain impacts inside of the skull resulting in shearing of brain tissue

most common for moderate - severe brain injuries

Can happen with external force

Question 21

Describe mild TBI (mTBI) concussion

Answer 21

(Glasgow coma scale 13-15)

Brief cognitive and physical rest
Most will recover, some will experience a protracted recovery, post-concussive syndrome
Second impact syndrome
Increase glucose metabolism and reduces energy reserve of brain tissue (excitotoxic metabolism)

Signs and symptoms:
Headache, dizziness, noise/light sensitivity, blurred vision, fatigue, irritability, anxiety, depression, cognitive dysfunction, sleep disturbance

Question 22

List synaptic neurotransmitter issues

Answer 22

1) acetylcholine-myasthenia Travis
2) dopamine-Parkinson’s disease
3) norepinephrine-depression
4) GABA-Huntington disease (overexcitation, inhibitory)
5) glutamate-ALS (excitatory)
6) serotonin-depression, anxiety

Question 23

Describe possible issue with upper and lower motor neurons

Answer 23

1) upper motor neuron (CNS):
Brain & spinal cord

Hyper reflexia, hypertonia (spasticity), spastic paralysis

2) lower motor neuron (PNS):
Spinal nerve roots & peripheral nerves

Hyporeflexia
Hypotonia
Flaccid paralysis

Question 24

Describe amyotrophic lateral sclerosis

Answer 24

(Aka Lou Gehrig disease)

Both upper and lower motor neurons

Devastatingly progressive, onset 50 yo or older, male > female

Unknown cause, some genetic component, proteinopathy in motor neurons

“Amyotrophic” muscle wasting (ant. Horn cell body)

Degenerative scarring “sclerosis” of lateral corticospinal tract

Diagnosis: nerve conduction test

Clinical presentation:
1) eye movement, bowel/bladder preserved
2) mixture of UMN and LMN
3) extremity weakness distally, cervical extensor weakness
4) cranial N nuclei for swallowing, chewing, facial weakness
5) eventual respiratory demise: 2-5 years

Medication:
1 that slows progression: riluzole

Question 25

describe Alzheimer’s disease

Answer 25

Females more prone. Some genetic connection, unknown exact cause. Accumulation of beta amyloid plaques which trigger further inflammation. Also, build up of Tao protein (inside neuron). This results in neurofibulary tangles in the neuron (toxic and disrupts neural connections). Progressive cortical atrophy. Some biomarker tests. No cure, some medications improve symptoms. Poor prognosis

Question 26

Describe movement disorder Parkinson’s Disease

Answer 26

• Unknown cause, proteinopathy
  alpha-synuclein and tau>disrupt
  Expressionless cellular process
• Neuroinflammation, degeneration
  of the substantia nigra (Basal
  Cognitive Ganglia)
• Decreased dopamine production dementia.

Relates to Relates to (basal ganglia). Affects posture, muscle tone. Substantia engraved specifically involved with dopamine production

• Hallmark characteristics:
  1) Tremor, rigidity, bradykinesia, postural instability (forward flexed), gait dysfunction (shuffling)
  2) Disorder of elderly (onset 50-60 yo), males>females, chronic degenrative neurological disease. Proteinopathy plays a role.
  3) masked face (expressionless)
  4) cognitive dysfunction with dementia
  5) Small voice volume, tiny writing

Treatment: Levodopa, deep brain
voice volume, tiny stimulation writing

Question 27

Describe Movement Disorder - Huntington Disease

Answer 27

• Progressive, hereditary disorder
  Average onset of symptoms age 40
  (Huntingtin gene) characterized by
  abnormalities of movement,
  personality and dementia.
• Treatment: Dopamine blocking agents-Haloperidol

Relates to (basal ganglia). Depletion of GABA. Increased dopamine (as if opposite of Parkinson’s). Excessive non intentional movement. Personality/behavior changes. Significant cognitive decline. Lethal condition with death 15-20 years after diagnosis. Some treatment with dopamine blocking agents but very little exist.

1) Average onset of symptoms age 40

2) Basal ganglia atrophy-caudate nucleus and putamen, depletion of GABA, increased dopamine

3) Chorea-involuntary, irregular, unpredictable muscle movements

4) Swallowing disorders, eye movement impairments, dysarthria

5) Wide based staggering gait

6) Neuropsych, intelectual disturbances

7) Death 15-20 years after dagnosis

Question 28

Describe multiple sclerosis

Answer 28

1) Sclerotic plaques develop throughout the CNS (brain and SC) => demyleinating
2) More common for people in the Northern Hemisphere, caucasian of Northern European decent
3) Onset teens through 35yo, women > men.
4) Genetic link , viral trigger

Optic neuritis, visual changes often the first sign

Spinal plaques may occur first

Fatigue-largest complaint

Heat increases weakness (Intolerance)

Cranial N involvement

Incoordination

Pain-neuropathic

Bowel and bladder

Question 29

List traumatic spinal cord injury types

Answer 29

Spinal cord at L2-L3

top 3 causes in order: 1) vehicular, 2) falls, 3) violence
VIP: they result in fractures that need to be fixated

1. Central Cord Syndrome
2. Brown-Séquard Syndrome
3. Anterior Cord Syndrome
4. Cauda Equina Syndrome

Question 30

Describe central cord syndrome

Answer 30

• Definition: Damage to the center of the spinal cord, often affecting motor function more in the arms than the legs.
  
  • mechanism: Hyperextension injuries, spinal stenosis, or trauma.
  • Signs & Symptoms: sensory and motor deficit in upper>lower extremities
  • prognosis: most have moderate but incomplete recovery
  • Physical Therapy Precautions: Avoid overstretching or aggressive movements in the neck; focus on progressive strengthening and functional mobility.

Question 31

Describe brown sequard syndrome

Answer 31

• Definition: Hemisection (one-sided damage) of the spinal cord causing asymmetric symptoms.
  
  • mechanism: Penetrating trauma
  • Signs & Symptoms:
    1) Ipsilateral (same side): Loss of motor function, vibration, sensation, and proprioception.
    2) Contralateral (opposite side): Loss of pain and temperature sensation.
  • prognosis: excellent, 99% ambulatory at final follow up
  • Physical Therapy Precautions: Focus on safety with mobility (due to sensory loss) and avoid positions that could worsen compression.

Question 32

describe anterior cord syndrome

Answer 32

• Definition: Damage to the anterior two-thirds of the spinal cord, sparing the posterior column.
  
  • mechanism: Flexion injuries
  • Signs & Symptoms:
  • bilateral Loss of motor function, pain, and temperature sensation
  • Proprioception and vibration are preserved.
  • prognosis: poor, 10-20% chance of motor recovery
  • Physical Therapy Precautions: Avoid activities that increase strain on the anterior cord; emphasize safety during mobility training.

Question 33

describe cauda equina syndrome

Answer 33

• Definition: Compression of the cauda equina nerve roots (below L2 level).
  
  • Cause: Herniated discs, trauma, tumors, or infection.
  • Signs & Symptoms:
  • Severe low back pain, leg weakness, saddle anesthesia, bowel/bladder dysfunction.
  • Treatment/Medication:
  • Emergency surgical decompression.
  • Pain management and anti-inflammatory medications.
  • Physical Therapy Precautions: Monitor for worsening neurological signs; avoid aggressive lumbar spine exercises post-surgery.

Question 34

What is the posterior part, corticospinal and spinothalamic part of the spinal tracts responsible for?

Answer 34

1) posterior part (dorsal column): sensory, vibration and proprioception.

2) Spinothalamic (sensory): pain and temp.

3) Corticospinal: motor

Question 35

Where does the dorsal column medial lemmiscal cross?

Answer 35

(Vibration, proprioception, light touch)

crosses higher up (medulla oblongata)

1. Sensory signals enter the spinal cord and ascend ipsilaterally (same side) in the dorsal columns (fasciculus gracilis for the lower body and fasciculus cuneatus for the upper body).
2. In the medulla, signals synapse in the nucleus gracilis and nucleus cuneatus.
3. After synapsing, axons decussate (cross) and ascend as the medial lemniscus to the thalamus.
4. Finally, the signals are relayed to the primary sensory cortex.

Question 36

Where does the (antero) lateral spinothalamic cross?

Answer 36

(Pain, temperature)

Crosses over right away (at spinal cord level)

1. Sensory signals enter the spinal cord and synapse with second-order neurons in the dorsal horn of the gray matter.
2. The second-order neurons decussate (cross) to the opposite side of the spinal cord through the anterior white commissure.
3. The signals then ascend contralaterally in the anterolateral tract (split into anterior and lateral spinothalamic tracts).
4. The pathway travels to the thalamus, where it synapses with third-order neurons.
5. The thalamus relays the signals to the primary sensory cortex for processing. Crosses over right away

Question 37

Where does the lateral corticospinal cross?

Answer 37

(voluntary motor)

Crosses over cervical area, higher up (medulla oblongata)

1. Motor signals originate from the primary motor cortex and descend through the internal capsule and brainstem.
2. At the medulla oblongata, approximately 85-90% of the fibers cross to the opposite side at the pyramidal decussation.
3. The crossed fibers descend in the lateral column of the spinal cord as the lateral corticospinal tract.
4. These fibers synapse with lower motor neurons in the anterior horn of the spinal cord, which then innervate the target muscles.

Question 38

what is the clinical presentation of traumatic spinal cord injuries?

Answer 38

Spasticity
Fatigue
Respiratory complications
Autonomic dysreflexia (common above T6)
Pressure ulcers
Skeletal changes, osteoporosis
Pain
Bowel, bladder, sexual dysfunction

Question 39

Explain Action Potential and Neurotransmission

Answer 39

An action potential is an electrical signal generated when a neuron reaches its threshold potential, causing sodium (Na⁺) channels to open, allowing Na⁺ to flow into the cell, depolarizing the membrane. This is followed by the opening of potassium (K⁺) channels, letting K⁺ out, repolarizing the membrane. The action potential travels along the axon to the synapse, where it triggers the release of neurotransmitters into the synaptic cleft. Neurotransmitters like glutamate (excitatory), GABA (inhibitory), dopamine, and serotonin modulate neuronal communication, influencing processes such as mood, movement, and cognition.

Question 40

Explain Glial Supporting Tissues in the CNS

Answer 40

The CNS is supported by several types of glial cells. Astrocytes maintain the blood-brain barrier, regulate nutrients, and support repair. Oligodendrocytes produce myelin sheaths to insulate axons and enhance signal conduction. Microglia act as immune cells, clearing debris and pathogens. Ependymal cells line the ventricles and produce cerebrospinal fluid (CSF). These glial cells are essential for maintaining homeostasis and supporting neuronal function.

Question 41

Explain Sensory vs. Motor Pathways

Answer 41

Sensory pathways (afferent) carry information from the body to the CNS, transmitting signals about touch, temperature, pain, and proprioception. These pathways ascend through structures like the dorsal column-medial lemniscal or spinothalamic tracts. Motor pathways (efferent) carry signals from the CNS to muscles, controlling voluntary and involuntary movements. The corticospinal tract is a primary motor pathway, with its fibers descending from the motor cortex to the spinal cord to stimulate muscle contractions.

Question 42

Explain Focal Effects of Brain Lesions

Answer 42

The effects of a brain lesion depend on the specific area damaged. For example, a lesion in the motor cortex can cause paralysis in specific body regions, while damage to Broca’s area affects speech production. Lesions in the occipital lobe impair vision, and those in the hippocampus affect memory. Focal lesions result in deficits tied directly to the functional role of the affected brain region.

Question 43

Explain Effects of Spinal Cord Injury by Location

Answer 43

The effects of a spinal cord injury depend on the level and completeness of the damage. Injuries at higher levels (e.g., cervical) can cause quadriplegia, while lower-level injuries (e.g., thoracic) may result in paraplegia. Damage to specific tracts affects their associated functions; for example, damage to the corticospinal tract causes motor deficits, while spinothalamic tract injuries impair pain and temperature sensation.

Question 44

Explain Causes and Effects of Increased Intracranial Pressure (ICP)

Answer 44

Increased ICP can result from trauma, tumors, infections, hydrocephalus, or hemorrhage, leading to pressure on the brain and reduced cerebral perfusion. Symptoms include headaches, nausea, vomiting, and altered consciousness. If untreated, increased ICP can cause brain herniation, leading to severe neurological deficits or death. Managing ICP requires addressing the underlying cause and reducing pressure through medical or surgical means.

Question 45

Describe the function of the ANS

Answer 45

Regulates activity of internal organs (glands, smooth muscles, cardiac muscles)
1. Sympathetic (SNS)- fight or flight
A. HR increase
B. Release glucose
C. Increases respiratory rate
D. Located in the T/S

2. Parasympathetic (PSNS)- Rest and Digest
   A. Conserves energy
   B. Decrease HR
   C. Decrease RR
   D. Removes waste
   E. Located in brainstem (cranial nerves) and sacral region (pelvic splanchnic nerves)

Question 46

List the cranial nerves and possible issues

Answer 46

I Olfactory - Sensory
* Sense of smell
* Deficit: loss of smell
II Optic- Sensory
* Vision
* Deficits: total/partial blindness
III Oculomotor- Motor
* proprioception of eye movement
* eye movement
* Contstriction of pupil
* Open/close eyelid
* Deficits: drooping eyelid, dilated pupil, loss of accommodation, double vision, inability to move eye in some directions, “affected eye drifts downward and outward”
IV Trochlear- motor
* motor eye
* Deficits: double vision, eye deviation upward, inability to move eye down and inward, head tilt forward and toward the normal eye
V Trigeminal- sensory
* Mastication
* Open/close mouth
* deficits: impaired sensation from upper face
Vl Abducens- motor (lateral eye movement)
* Inability to move eye laterally
* Affected eye turns inward at rest
VII Facial- motor
* facial expression
* 2/3 of tongue (taste)
* Deficits: asymmetry
VIII- Vestibulocochlear - sensory
* equilibrium
* Hearing
* Deficits: impaired hearing, vertigo, tinnitus, nystagmus
IX Glossopharygeal- sensory
* 1/3 taste to posterior tongue
* Swallowing
* Deficits: difficulties swallowing, speaking
X Vagus- motor
* swallowing
* Speech
* Parasympathetic
* Deficits: loss of voice, impaired gag reflex, difficulties swallowing
* Say “ah”
XI Accessory- Motor
* inntervates SCM and UT
* Muscle weakness
XII Hypoglossal- motor
* Tongue movement
* Deficits: tongue deviates towards the affected side

Question 47

What are the types of sensory and tactile receptors?

Answer 47

Sensory:
1) Mechanical Stimuli:
Pressure
Stretch
Vibration
Movement
2) Tactile receptors:
merkel’s discs
Unencapsulated
Slowly-adapting
Light touch
Small receptive fields (vibrations)
3) Pacinian Corpuscles:
Encapsulated
Rapidly-adapting
Heavy pressure
Large receptive fields (vibrations)
4) Meissner’s Corpuscles:
Encapsulated
Rapidly-adapting
Light touch
Small receptor fields (vibrations)
5) Ruffini’s Corpuscles:
Encapsulated
Slowly-adapting
Heavy pressure
Large receptor field (vibrations)

Question 48

Explain the neuroendocrine behavioral responses

Answer 48

sympathetic (sympathetic ganglia: prevertebral, end organs, adrenals): T1 - L3

Parasympathetic (in or near end organs): S2 - S4 and CN III, VII, IX, X

Question 49

What are the classes of peripheral nerve injury?

Answer 49

class 1 (Neuropraxia): reversible conduction block resulting from ischemia or demyelination

Class 2 (axonotmesis): axon interruption but basal lamina remains intact

Class 3 (neurotmesis): nerve fiber and basal lamina interruption (complete nerve severance)

Question 50

Describe diabetic polyneuropathy

Answer 50

Presents with stocking & glove, deep ache, burning pain

It is characterized by damage to the cells of the peripheral nerves, primarily Schwann cells and neurons, caused by the metabolic effects of high blood sugar (hyperglycemia), leading to impaired insulin signaling, oxidative stress, inflammation, and ultimately disruption of nerve function and structure, often manifesting as impaired axonal transport, demyelination, and neuronal death.

(Stable blood glucose is key)

a. KEY CELLULAR POINTS:
1. ADVANCED GLYCATION END PRODUCTS (AGES): Excess glucose in the blood reacts with proteins, creating AGEs which accumulate in nerve cells, disrupting their function and contributing to oxidative stress
2. POLYOL PATHWAYS ACTIVATION: Hyperglycemia can activate the polyol pathway, causing an imbalance in the production of certain sugar alcohols which can damage nerve cells.
3. MITOCHONDRIAL DYSFUNCTION: High glucose levels can disrupt mitochondrial function, leading to increased production of reactive oxygen species (ROS) and further oxidative stress.
4. IMPAIRED INSULIN SIGNALING: Diabetes disrupts insulin signaling in the peripheral nerves, leading to decreased neurotrophic support and impaired nerve cell survival.
5. SCHWANN CELL DAMAGE: Schwann cells, responsible for myelins production in peripheral nerves, as particularly vulnerable to hyperglycemia, leading to demyelination and impaired nerve conduction.
6. MICROVASCULAR CHANGES: diabetic microangiopathy, characterized by damage to small blood vessels in the nerves, can restrict blood flow and oxygen delivery to the nerve cells, further contributing to their damage.
damage: axonal
7. Consequences of cellular damage: axonal damage, demyelination, neuronal apoptosis, neuroinflammation
b. S/S: pain, numbness, tingling or burning in the hands, feet, or legs. Digestive issues, urinary problems, dizziness, and sexual dysfunction
c. Causes: high blood sugar levels
d. Tx: lifestyle changes, insulin
e. PT: strength, endurance, ROM, mobility, cardiovascular conditioning

Question 51

describe carpal tunnel syndrome

Answer 51

(median nerve neuropathy)

Chronic repetitive overuse, acute trauma, 70% women, associated with DM, alcoholism, hypothyroidism, pregnancy

• Definition: A condition caused by compression of the median nerve as it passes through the carpal tunnel in the wrist.
• Cause: Repetitive wrist movements, prolonged wrist flexion/extension, pregnancy, or conditions like diabetes and rheumatoid arthritis.
• Signs & Symptoms: Numbness, tingling, and pain in the thumb, index, middle, and part of the ring finger; weakness in grip strength and difficulty with fine motor tasks.
• Treatment/Medication: Conservative treatment includes wrist splints, NSAIDs for pain, corticosteroid injections, or surgery for severe cases (carpal tunnel release).
• Physical Therapy Precautions: Avoid aggravating repetitive wrist motions or prolonged compression. Focus on wrist mobility, nerve gliding exercises, and ergonomics to reduce strain.

Question 52

Describe thoracic outlet syndrome

Answer 52

structures involved:
Brachial plexus, subclavian artery, hypertrophy of scalene muscle, first rib, pec minor

• Definition: A condition caused by compression of nerves or blood vessels (brachial plexus, subclavian artery, or vein) as they pass through the thoracic outlet between the clavicle and first rib. Causing pain, parenthesis is
• Cause: Poor posture, repetitive overhead movements, trauma, congenital abnormalities (e.g., cervical rib), or tight muscles (e.g., scalene or pectoralis minor).
• Signs & Symptoms: Pain, numbness, and weakness in the arm or hand, often worsened by overhead activity; in vascular TOS, there may be swelling, discoloration, or a weakened pulse.
• Treatment/Medication: Adson maneuver
  Conservative treatment includes physical therapy for postural correction, stretching, and strengthening; NSAIDs or muscle relaxants for pain; surgical decompression for severe cases.
• Physical Therapy Precautions: Avoid prolonged overhead activities and positions that exacerbate symptoms. Focus on gentle stretching, nerve gliding, and posture correction exercises.

Question 53

Describe Complex Regional Pain Syndrome (CRPS)

Answer 53

• Definition: A chronic pain condition characterized by disproportionate and persistent pain, usually affecting a limb, following injury or trauma.
• Cause: Abnormal nerve response after injury, surgery, or immobilization; the exact cause is unclear but involves dysfunction of the central and peripheral nervous systems.
• Signs & Symptoms: (Cycle of pain and swelling), pain out of proportion to injury, burning pain, sympathetic NS in overdrive, sensory disruption, trophic changes in tissue (texture, color, sweating, goosebumps), discoloration due to vasomotor abnormality, sometimes follows cast removal
• Treatment/Medication: Multidisciplinary approach including pain medications (NSAIDs, corticosteroids, or nerve blocks), physical therapy, desensitization techniques, and sometimes psychological support. In severe cases, spinal cord stimulation may be considered.
• Physical Therapy Precautions: Avoid overly aggressive exercises that increase pain. Focus on gentle, gradual movement, desensitization, and functional restoration to prevent worsening symptoms or further disuse.

Question 54

Describe Guillain Barre Syndrome

Answer 54

AIDP Acute Inflammatory Demyelinating Polyradiculoneuropathy:
* Immune mediated * Often follows viral infection * Ascending, symmetrical paralysis * Decline over 2-4 weeks, plateau, recovery * Risk of respiratory demise * Treatment: IVIG, plasmapheresis

It is characterized by an autoimmune response where the body’s immune system mistakenly attacks the myelin sheath surrounding the peripheral nerves, causing inflammation and damage to the nerve fibers, primarily by infiltrating immune cells like T cells and macrophages into the peripheral nerves, leading to disruption of nerve signal transmission and resulting in muscle weakness and
paralysis.
a. KEY CELLULAR POINTS:
1. MOLECULAR MIMICRY: Often triggered by a preceding infection, where a virus or bacteria shares similar molecular structures with components of the myelin sheath, causing the immune system to mistakenly target the nerve tissue.
2. AUTOREACTIVE ANTIBODIES: the immune system produces antibodies that bind to specific proteins on the myelin sheath (like gangliosides), leading to the destruction of the myelin and subsequent damage to the axon.
3. IMMUNE CELL INFILTRATION: activated T cells (CD4+ helper T cells) and macrophages migrate to the peripheral nerves, causing inflammation and directly attacking the myelin sheath.
4. DEMYELINATION
5. AXONAL DAMAGE
6. CELL TYPES INVOLVED IN GBS: Schwann cells, T lymphocytes (T cells), macrophages, B lymphocytes (B cells)
b. S/S: pins and needles in the fingers, toes, ankles, and wrist, weakness in the legs that spread to the upper body, gait deficits, trouble with facial movements, including speaking, chewing, swallowing, double vision or inability to move eyes, severe pain, trouble with bladder control or bowel control, rapid HR, low or high BP, trouble breathing
c. Types:
1. Acute inflammatory demyelinating polyredculoneuropathy (AIDP), Miller Fosher syndrome (MFS), Acute motor axonal neuropathy (AMAN)
or acute motor-sensory axonal neuropathy (AMSAN)
d. causes: infection with campylibacter, a type of bacteria often found in undercooked poultry. Influenza virus, cytomegalovirus, Epstein-Barr virus, Zika virus, Hepatitis A, B, C, and E, HIV (AIDS), etc.
e. Dx: spinal tap, electromyography, nerve conduction studies.

Question 55

Describe Post-Polio Syndrome

Answer 55

(New neuromuscular symptoms decades after recovery from polio. Fatigue, weakness, decreased function, pain. Compensated over sprouting motor neurons can no longer maintain the motor unit. Energy conservation, supportive care)

It is a gradual deterioration of motor neurons in the spinal cord that were damaged by the polio virus, leading to a situation where the remaining healthy neurons had compensated by sprouting new nerve fibers to reinnervate muscles, eventually becoming overloaded and begin to weaken, causing muscle atrophy and progressive weakness due to a decline in the ability to maintain these new never connections; essentially, the “re-wired” nervous system starts to fail after years of overworking to compensate for the initial damage.
a. S/S: muscle weakness, atrophy, or loss of function, joint pain and tightness, chronic fatigue, swallowing and speech problems, respiratory problems, cramps and muscle twitching, sensitivity to cold temperatures
b. Cause: Polio virus
c. Dx: EMG, MRI, muscle biopsy, blood test
d. PT: strengthening, flexibility, ROM, cardiovascular endurance, bracing and AD

Question 56

Describe Myasthenia Gravis-Motor End Plate Disorder

Answer 56

It is an autoimmune disease that affect the neuromuscular junction (NMJ)
1. ANTIBODIES: MG is caused by autoantibodies that target the nicotine acetylcholine receptors (AChR) or other components of the postsynaptic muscle endplate at the NMJ. These antibodies prevent acetylcholine from attaching to its receptors, which impairs neuromuscular transmission and causes muscle weakness.
2. T CELLS: CD4+ cells play a role in MG, secreting cytokines that regulate B cell antibody production. In MG patients, CD4+ FoxP3+ regulatory
T cells (Treg) are functionally defective.
3. B CELLS: MG is a B cell mediated autoimmune disorder
THYMUS: Thymus changes have been observed in patient with early onset MG, such as hyperplastic medullary epithelial cells, germinal centers, and complement deposition.
4. S/S: Drooping of one or both eyelids (Ptosis), double vision (diplopia), difficulties speaking, swallowing, chewing, facial expressions
5. Dx: Neurological exams, Ice pack Test, blood analysis, repetitive nerve stimulation, single fiber EMG, CT, MRI, pulmonary function test
6. Tx: Cholinesterase inhibitors, corticosteroids, immune suppressants
7. PT: strength, ROM, cardiovascular conditioning, mobility
8. decreased production of Acetylcholine:
A. MENTAL: delirium, agitation, visual hallucinations, rapid speech, memory decline, difficulty recalling words, and learning difficulties.
B. PHYSICAL: Flushed skin, dry mouth and throat, blurred vision, increased sensitivity to light, weakness in the arms, legs, and hands, low muscle tine, constipation, and difficulty breathing
C. Other S/S: fever, nausea and vomiting, diarrhea, slow heart rate and difficulty urinating
D. ASSOCIATED CONDITIONS: Alzheimer’s disease, Lambert-Eaton myasthenia syndrome, Myasthenia Gravis, Aging, Exposure to pesticides and insecticides

Question 57

Summarize Myasthenia Gravis-Motor End Plate Disorder

Answer 57

Most common disorder
of neuromuscular transmission

Fluctuating weakness and fatiguability of skeletal muscle

Women in 20’s-30’s
Men in 50’s-60’s

Autoimmune disorder, thymus gland plays a role

DM, RA, SLE, thyroid disease

Anti ACh antibodies block the acetylcholine binding for muscular
contraction

Cranial muscle weakness: diplopia, ptosis

Thymectomy, Corticosteroids