Unit 5: CHapter 15

Question 1

Motor Cortex

Answer 1

Represents the highest level of motor function.

The primary, premotor, and supplementary motor cortices located in the posterior part of the frontal lobe initiate and control precise, skillful, and intentional movements of the distal and especially flexor muscles of the limbs and speech apparatus.
Receives information directly from the thalamus and somatosenspry cortex and indirectly from the cerebellum and basal ganglia.

Question 2

Primary Motor Cortex

Answer 2

The motor strip
Is situated on the rostral surface and adjacent portion of the central sulus.
Controls muscle movement sequences and is also the fistrt level of descending control and precise motor movements.
Aids in control of the muslce of the hands, farcical expression and speech

Question 3

Motor Homunculus

Answer 3

Known as the neurons in the primary motor cortex that are arranged in a distorted map of the body.

Question 4

Premotor Cortex

Answer 4

Located anterior to the primary motor cortex and mainly Innervated the primary motor strips
Produces more complex patterns of movement

Question 5

Supplementary Motor Cortex

Answer 5

Located on the medial surface in the pre motor region.
Important for performance of complex skillful movement that involve both sides of the body

Question 6

Upper Motor Neuron

Answer 6

Exert control over the LMNs
Project from the motor strips in the cerebral cortex to the ventral horn and are fully contained in the CNS

Question 7

Myasthenia Gravis

Answer 7

is a disorder of NMJ transmission due to antibody-mediated attack on nAChR or muscle-specific tyrosine kinase.
This autoimmune disease may occur at any age, with peak incidence in young adulthood, and is three times more common in females than males.

Question 8

Myasthenia Gravis Manifestation

Answer 8

have reduced postsynaptic membrane area and fewer AChR, each release of ACh from the presynaptic membrane results in a lower-amplitude end-plate potential.
This causes weakness and fatigue with sustained effort. The eye and periorbital muscles are commonly affected, with ptosis due to eyelid weakness or diplopia due to extraocular muscle weakness as an initial symptom. Chewing and swallowing may be difficult.
Weakness in limb movement usually is more pronounced.

Question 9

Carpel Tunnel Syndrome

Answer 9

Common compression type mono neuropathy
Caused by compression of the medial nerve as it travels with the flexor tendons through a canal made by the carpel bones and transverse carpel ligament.

Question 10

Carpal Tunnel Syndrome

Answer 10

Characterized by pain, paresthesia, and numbness of the thumb and first two and one-half digits of the hand; pain in the wrist and hand, which worsens at night; atrophy of the abductor pollicis muscle; and weakness in precision grip.
These abnormalities may contribute to clumsiness of fine motor activity.

Question 11

Tinea SIgn

Answer 11

Is a tingling sensation radiating int he palm elicited by light percussion over the medial nerve at the wrist

Question 12

Gillian-Barre Syndrome

Answer 12

acute immune-mediated polyneuropathy.
Several indices of the disorder, including pure motor axonal degeneration and axonal degeneration of both motor and sensory nerves.
It is caused by infiltration of mononuclear cells around the capillaries of peripheral neurons, edema of the endoneurial compartment, and demyelination of ventral spinal roots.
likely has an immune component.

Question 13

Gillian Barre Syndrome Manifestations

Answer 13

Progressive ascending muscle weakness of the limbs, producing a symmetric flaccid paralysis, characterizes the disorder.
Symptoms of paresthesia and numbness often accompany loss of motor function.
A ventilator is required if paralysis involves respiratory muscles.
ANS involvement: causes postural hypotension, arrhythmias, facial flushing, abnormalities of sweating, and urinary retention is common.
Pain is a common feature.

Question 14

Back Pain

Answer 14

result from many interrelated problems involving spinal structures and spinal nerve roots.
Low back pain frequently experience musculoligamentous injuries and age-related degenerative changes in the intervertebral disks and facet joints.
Other causes include disk herniation, which is a herniated nucleus pulposus and spinal stenosis, which is characterized by narrowing of the central canal, typically from hypertrophic degenerative changes.
Risk Factor: heavy lifting, smoking and obesity

Question 15

Parkinson’s Disease

Answer 15

Degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity, akinesia/bradykinesia, and postural changes.
characterized by progressive destruction of the nigrostriatal pathway and reduction in striatal dopamine.
Brain Abnormaility: degeneration of the pigmentation nigrostriatal dopamine neurons.
Residual nerve cells contain Lewy bodies.

Question 16

Lewy Bodies

Answer 16

Are produced inside degenerated neurons ion many people with PD or Parkinsonism.

Question 17

PD Causes

Answer 17

Interaction of enviromental and genetic factors

Question 18

Parkinsonism

Answer 18

Clinical syndrome arising from degenerative changes in basal ganglia function.
Can also develop as a postencephalitic syndrome, a side effect of antipsychotic drugs that block dopamine receptors, a toxic reaction to a chemical agent, or an outcome of severe carbon monoxide poisoning.

Question 19

PD Manifestations

Answer 19

most visible manifestation of the disorder and affects mainly the hands and feet; head, neck, face, lips, and tongue; or jaw.
characterized by rhythmic, alternating flexion and contraction movements (4 to 6 beats/minute) that resemble rolling a pill between the thumb and forefinger. The tremor is initially unilateral, occurs when the limb is supported and at rest, and disappears with movement and sleep. The tremor eventually progresses bilaterally.

Question 20

Amyotrophic Lateral Sclerosis (ALS)

Answer 20

also known as Lou Gehrig disease, is a devastating neurologic disorder that selectively affects motor function.
Affects the LMNs of the spinal cord, the motor nuclei of the brain stem, particularly the Hypoglossal nuclei and the UMNs of the cerebral cortex
Extensive in distal parts of the affected tracts do neurons under dengue ration at the distraction terminals.

Question 21

ALS Manifestations

Answer 21

may be due to UMN or LMN involvement.
UMN lesions include weakness, spasticity or stiffness, and impaired fine motor control.
Dysphagia, dysarthria, and dysphonia may result from brain stem LMN involvement or from dysfunction of UMNs descending to the brain stem.
LMN lesions include fasciculations, weakness, muscle atrophy, and hyporeflexia.
Muscle cramps involving the distal legs often are an early symptom.
The most common clinical presentation is slowly progressive weakness and atrophy in distal muscles of one upper extremity, followed by regional spread of clinical weakness.

Question 22

Multiple Sclerosis (MS)

Answer 22

inflammation and destruction of mostly the CNS myelin.
The peripheral nervous system is spared, and there is usually no evidence of an associated systemic disease.
Likely immune mediated disorder occurring in genetically susceptible people
Target antigen is unknown but suggests immune response to a CNS protein.

Question 23

MS Stages

Answer 23

1. first stage that involves the sequential development of small inflammatory lesions
2. second stage during which the lesions extend and consolidate and when demyelination and gliosis (scar formation) occur
   It is not known whether the inflammatory process, present during the first stage, is directed against myelin or against the oligodendrocytes that produce myelin.

Question 24

MS Manifestations

Answer 24

involves the demyelination of nerve fibers in the white matter of the brain, spinal cord, and optic nerve.
CNS myelin is formed by oligodendrocytes, chiefly those lying among the nerve fibers.
The properties of the myelin sheath—high electrical resistance and low capacitance—permit it to function as an electrical insulator.
Demyelinated nerve fibers display conduction abnormalities ranging from decreased velocity to conduction blocks.

Question 25

Inferferon Beta Treatment for MS

Answer 25

A cytokines that act as an immune enchancer. Injected and tolerated Side effects: flu like symptoms for 24 to 48 hrs

Question 26

Spinal Cord Injury

Answer 26

Most involve damage to the vertebral column or supporting ligaments and spinal cord. Commonly have both sensory and motor function. Most are due to writhing movement and a compressive force

Question 27

Injury to the Vertebral Column

Answer 27

Include fractures, dislocations and subluxations # can occur at any part of the bony vertebrae, causing fragmentation of bone. It most often involves the pedicle, lamina, or facets. Dislocation or subluxation injury displaces vertebral bodies, with one overriding another and misalignment of the vertebral column. Damage to the ligaments or bony vertebrae may make the spine unstable.

Question 28

Flexion Injury of the Spine

Answer 28

Occur when forward be binding of the spinal column exceeds normal movement limits. More common ion the C4-C6.

Question 29

Extension Injury’s of the the Spine

Answer 29

Occur with excessive forced being of the spine backwards Typical extension injury involves a fall in which the chin or face is the point of impact causeing hyperextension of the neck. More common in C4-C6

Question 30

Compression Injury of the Spine

Answer 30

Causing the vertebral bones to shatter, squash or even burst occurs when there is spinal loading from a high velocity blow to the top of the head, such as a diving injury. May occur with conditions such as osteoporosis and bone metastasis

Question 31

Tetraplegia or Quadriplegia

Answer 31

is the impairment or loss of motor and/or sensory function after damage to neural structures in the cervical segments of the spinal cord. It results in impairment of function in the arms, trunk, legs, and pelvic organs.

Question 32

Paraplegia

Answer 32

refers to impairment or loss of motor and/or sensory function in the thoracic, lumbar, or sacral segments of the spinal cord from damage of neural elements in the spinal canal. Arm functioning is spared, but depending on the level of injury, functioning of the trunk, legs, and pelvic organs may be impaired. includes conus medullaris and cauda equina injuries.

Question 33

Complete Cord Injuries

Answer 33

Severance of the cord, disruption of nerve fibers or interruption of blood supply to that segment resulting in complete destruction of neural tissue and UMN or LMN paralysis No motor function is preserved in segments S4-S6

Question 34

Incomplete Cord Injuries

Answer 34

Imply residual motor or sensory function below the level of injury. Prognosis is better because of preservation of axonal function.

Question 35

Autonomic Dysreflexia

Answer 35

also known as autonomic hyperreflexia, represents an acute episode of exaggerated sympathetic reflex responses in people with injuries at T6 and above, in which CNS control of spinal reflexes is lost. It does not occur until spinal shock has resolved and autonomic reflexes return, most often within the first 6 months after injury. It is most unpredictable during the first year after injury, but can occur throughout the person’s lifetime.

Question 36

Autonomic Dysreflexia Manifestations

Answer 36

is characterized by mild to severe hypertension, skin pallor, and the piloerector response. Because baroreceptor function and parasympathetic control of heart rate travel by way of the cranial nerves, these responses remain intact. Continued hypertension produces a baroreflex-mediated vagal slowing of the heart rate to bradycardic levels. There is an accompanying baroreflex-mediated vasodilation, with flushed skin and profuse sweating above the level of injury, headache ranging from dull to severe, nasal stuffiness, and feelings of anxiety. A person may experience one, several, or all of the symptoms with each episode.