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Advanced Pathophysiology > Module 3 Chapters 15 & 16 Disorders of Motor and Brain Function and Disorders of Brain Function > Flashcards

Module 3 Chapters 15 & 16 Disorders of Motor and Brain Function and Disorders of Brain Function Flashcards

1
Q

What is the motor unit?

A

A motor unit consists of a motor neuron and all the muscle fibers it innervates.

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2
Q

How does a motor unit control skeletal muscle movement?

A

Whenever the motor neuron develops an action potential, all the muscle fibers that the motor neuron innervates develop action potentials. This leads all the muscle fibers contracting at once, working to move the bones they are attached to.

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3
Q

Describe the hierarchy of the motor control system

A

The frontal lobe houses the premotor cortex, this is where planning and purpose of movement originates. Considered the highest level of motor functioning.

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4
Q

Where is the premotor cortex? What does it do?

A

The premotor cortex is located in the frontal lobe. Planning and purpose of movements originates here. It is considered the highest level of motor function.

Controls complex patterns of movements

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5
Q

Where is the motor cortex? What does it do?

A

Also located in the frontal lobe. Has a close relationship with the premotor cortex. Controls body movement.

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6
Q

What is the somatosensory cortex/association area? Where is it?

A

This is located in the parietal lobe, at the top of the brain. It is right next to the motor cortex in the frontal lobe. The somatosensory cortex/ association area receives sensory information from the periphery, processes it and sends that information to the motor and premotor cortex.

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7
Q

What areas of the body take up the most primary motor cortex space?

A

The hands, face, and speech take up over half of the primary motor cortexes SA.

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8
Q

What is the pyramidal motor system? Why is it called this? What does it control? Where do each of these originate?

A

The pyramidal motor system is a pyramid shaped network of neurons with the apex located in the motor cortex. These motor tracts are further subdivided into the
1. Pyramidal - controls delicate muscle movement. Voluntary movement. Called pyramidal because they pass through the pyramids of the medulla.
2. Extrapyramidal - crude, supportive movement patterns.
based on the location of their decussation. Involuntary movement.
The P system originates in the motor cortex while the EP system originates in the basal ganglia (brainstem).

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9
Q

How do disorders of the pyramidal tract present? What about the extrapyramidal?

A

P - spasticity and paralysis. Think of stroke.

EP - involuntary movements, rigidity, immobility.

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10
Q

What does the cerebellum do in regard to movement?

A

Primary role is controlling balance and coordination.

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11
Q

How do muscles and nerves communicate?

A

The motor unit - neuron and the muscles fibers it innervates.

Each of those contact points between the neuron and the muscle have a neuromuscular junction.

The neuron communicates by sending out neurotransmitters which the muscle receptors pick up and respond to.

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12
Q

What is an axon terminal?

A

The portion of the neuron that makes the closest contact with the muscle at the neuromuscular junction. This is where neurotransmitters are released from so the two can communicate.

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13
Q

What neurotransmitter is used at the neuromuscular junction? How does this affect the muscles?

A

Acetylcholine. Ach binding at the site of the neuromuscular junction results in muscle contraction.

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14
Q

Muscular atrophy. What is it? What causes it?

A

Shrinking of muscle cells due to reduced use or reduced nutrition. The body wants to be as efficient as possible. Cells that are too big for their current job expend more energy. The body adapts to this and reduces energy expenditure.

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15
Q

Muscular dystrophy

A

Genetic disorder that results in the progressive deterioration of skeletal muscle. Considered a disorder of mixed muscle deterioration due to a combination of hypertrophy, atrophy, and necrosis of muscle cells.

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16
Q

What happens to damaged peripheral nerves? What are common causes?

A

Damaged peripheral nerves undergo degenerative changes followed by degradation of the myelin sheath fibers.

Common causes include trauma and poorly controlled DM (neuropathy).

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17
Q

Can peripheral nerves regenerate?

A

Yes, depends on the proximity to the soma (cell body).

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18
Q

Curare

A

A naturally found neuromuscular junction blocking agent. Collected from dart frogs. Many drugs have been developed from it.
Roc is one of them. Vec.

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19
Q

How does clostridium botulinum affect Ach? What is this?

A

Blocks ACH resulting in paralysis. A type of food poisoning.

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20
Q

Myasthenia Gravis
1. What is it?
2. Patho
3. Thymus
4. Who is affected most often?

A
  1. An autoimmune disorder that affects the neuromuscular junction.
  2. A reduction in the number of Ach receptors at the neuromuscular junction. This reduction in number is caused by host antibodies destroying these receptors.
  3. Enlarged in these patients
  4. Young women and older men are most commonly affected
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21
Q

What is the thymus? Where is it? What happens to it as we age? How is this observed for with MG?

A

Large role in immunity in early childhood. Teaches the developing body immunocompetence. Located high up near the sternum. Shrinks as we age, and the immune system starts to know what to do. CT or MRI of the chest can locate enlarged thymus gland and help dx the disease.

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22
Q

Clinical manifestations of myasthenia gravis? What causes these symptoms?

A
  1. Muscle weakness with exercise or repetitive muscle movement. This is caused by the limited number of ACH receptors being occupied.
  2. Difficulty with eye movement, swallowing, talking, handling oral secretions. All of these tasks require ach to maintain. Over time ach gets used up.
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23
Q

How is MG diagnosed?

A
  1. Neurological exam
  2. Blood studies looking for the AChR antibodies - the antibodies responsible for destroying the receptors at the neuromuscular junction site.
  3. Repetitive nerve conduction studies - EMG
  4. Tensilon or edrophonium test for classic dx.
  5. CT or MRI of the chest - looking for enlarged thymus (thymoma)
  6. Thyroid function test - mainly a RO exam
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24
Q

How is MG managed?

A
  1. Immunosuppression - stop the body from attacking the Ach receptors.
  2. Steroids - reduce inflammation and reduce the body’s immune response.
  3. Anticholinesterases - prevent the breakdown of Ach allowing more of the neurotransmitter to be present in the body.
  4. Plasmapheresis - clears the body of antibodies
  5. IVIG
  6. Thymectomy
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25
Q

Myasthenic crisis
1. Main concern?

A

Not enough medications - not enough Ach in the body. Exacerbation of the body weakness secondary to repetitive muscle use.
1. Main concern - respiratory status.

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26
Q

Cholinergic crisis

A

Too much medications - too much Ach
Lots of secretions, perspiration, abdominal cramping, diarrhea.

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27
Q

Mononeuropathies

A

Peripheral neuropathy that affects one nerve.

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28
Q

Polyneuropathy

A

Peripheral neuropathy, typically involves demyelination. If the demyelination occurs in a higher up part of the motor/sensory system. The higher up it occurs, the more downstream effects will be experienced.

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29
Q

How does neuropathy present in the beginning?

A

Distal moving proximal

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30
Q

What causes polyneuropathy?

A
  1. Immune mechanisms (GBS) - the immune system mistaking attacks the myelin sheaths resulting in demyelination. Occurs distal to proximal.
  2. Toxic agents (lead. alcohol, arsenic)
  3. Metabolic diseases (DM, uremia)
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31
Q

What are the basal ganglia? Roles?

A

A group of deep, interrelated subcortical nuclei that control movement. Receives input from cerebellum, sensory systems, and motor cortex.

Plays a role in motor movements, habit forming, procedural learning, eye movements and others. “Muscle memory”.

Located deep in the center of the brain

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32
Q

Basal Ganglia disorders, what will be seen?

A

Think of extrapyramidal - because they are the highest part of the EP system where decussation occurs.

  1. Involuntary movements
  2. Alterations in muscle tones - rigid/stiff/flaccid at inappropriate times
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33
Q

Tremor

A

involuntary, oscillating contractions of opposing muscle groups around a joint

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34
Q

Tic

A

involuntary twitch

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35
Q

Chorea

A

irregular wriggling and writhing movements

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36
Q

athetosis

A

continuous wormlike, twisting, and turning movements

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37
Q

Ballismus

A

violent, sweeping, flinging movements

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38
Q

Dystonia

A

simulataneous contraction of agonist and antagoinst muscles, contortion

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39
Q

Dyskinesias

A

Frequent involuntary movement of muscles typically face.

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40
Q

Parkinson’s Disease
1. What is it?
2. Patho
3. What problems are seen with PD?

A
  1. Degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity, and bradykinesia. EP.
  2. Caused by the destruction of nigrostriatal pathway leading to a reduction in striatal concentrations of dopamine.
  3. Fatigue, slight tremor, decrease in manual dexterity. Muscle rigidity. Changes in facial expression. Uncontrolled drooling. Dementia. Excessive sweating. Orthostatic hypotension.
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41
Q

What neurotransmitter is deficient in Parkinson’s disease?

A

Dopamine is deficient in Parkinson’s disease. This is a widely used neurotransmitter in the extrapyramidal pathway.

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42
Q

How is Parkinson’s disease treated?

A
  1. Dopamine agonists - pramipexole (mirapex) and Ropiniole (Requip) are commonly used ones. These increase the amount of dopamine avaliable for the basal ganglia.
  2. Dopamine receptor antagonists
  3. COMTs
  4. Deep brain stimulator
  5. Sterotactic palliotomy
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43
Q

Where are the upper motor neurons (UMN) and the lower motor neurons (LMN)? What is their function?

A

The UMN originate in the cerebral cortex and travel down to the brain stem or the spinal cord. Here they connect with the LMN to send along impulses of voluntary movement.

The LMN are located in the spinal cord and brainstem and travel throughout the spinal cord, innervating glands and muscles. They send the voluntary muscle impulse along that results in movement or release.

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44
Q

Motor neuron disease
1. What is affected?
2. Examples

A
  1. Progressive degeneration of the upper or lower motor neurons.
  2. ALS, Polio, progressive spinal muscular atrophy
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45
Q

What is the stretch reflex? What can affect it?

A

AKA myotatic reflex. Helps maintain muscle tone. Disorders of the LMN can alter the spinal reflexes including the stretch reflex.

46
Q

What is Amyotrophic Lateral Sclerosis? Progression? Patho?

A

ALS - a progressive disease of the motor function both UMN and LMN are affected. Brain remains largely unchanged.

Average survival is 2-5 years from onset of symptoms.

This occurs due to degradation of motor neurons leading to reduced muscle stimulation leading to muscle atrophy leading to weakness.

47
Q

What neurons are most commonly affected with ALS?

A

The anterior horn cells of the spinal cord
This affects the motor nuclei of the brain stem which has a large effect on the hypoglossal nerve’s ability to function.

48
Q

Clinical manifestations of ALS

A
  1. Limb cramping and weakness
  2. Poor coordination
  3. Slurring of speech - hypoglossal
  4. Trouble swallowing - exacerbates atrophy
  5. single muscle group paresis that spreads
  6. Hypotonia - low muscle tone
49
Q

How is ALS treated?

A

Riluzole (Rilutek) - antiglutamate - prolongs doesn’t cure.

50
Q

What major issues can occur with ALS?

A

Trouble swallowing and weakened muscles can lead to aspiration and pneumonia. Decreased ability to cough and manage oral secretions can lead to resp issues.

51
Q

Multiple Sclerosis
1. What is affected? What is going on?
2. Causes? Who is most commonly affected?
3. How does the disease progress?

A
  1. MS is a disease of CNS demyelination.
  2. Most commonly affects young and middle-aged adults. Nontraumatic causes.
  3. MS presents with a pattern of relapsing-remitting occurrences. At first the patient is able to return to normal or near-normal neurological functioning, but as the disease progresses improvement between exacerbations decreases.
52
Q

What is the pathophysiology behind MS?

A

Causes a demyelination of the CNS. The lesions of demyelination are randomly distributed throughout the brainstem, spinal cord, and cerebellar peduncles.

Initially only the myelin sheaths can be affected, but as the disease progresses destruction of neurons and their parts can occur resulting in more exaggerated symptoms.

53
Q

Clinical manifestations of MS
1. Early
2. Late

A
  1. Early -
    - Weakness, numbness, or both
    - 50% start with symptoms in one limb while the other half experience symptoms bilaterally
    - tingling of extremities, tight-band like sensation around the trunk - r/t posterior involvement of the spinal cord
  2. Progressive
    - Symmetrical or asymmetrical development of paraplegia, paraparesis, ascending paresthesia, loss of deep sensation in feet, sphincteric dysfunction, bilateral Babinski signs.
54
Q

How is MS diagnosed?

A

CT scan or MRI - looking for areas of loss of white matter
LP - looking for certain proteins in the CSF

55
Q

MS treatment

A

Drug therapy is divided into three categories:
1. Acute treatment - steroids, pheresis, IVIG
2. Disease modifying - interferon beta, mitoxantrone
3. Symptom treatment - Dantrolene, baclofen, diazepam (spasticity), cholinergic drugs for bowel and bladder issues, antidepressants.

56
Q

Spinal cord injuries
1. Where do flexion/extension injuries occur most often on the spinal cord?
2. Central cord syndrome
3. Brown-Sequard Syndrome
4. Anterior cord syndrome
5. Posterior cord syndrome

A
  1. Cervical spine (C4-C6)
  2. CCS - incomplete injury of the spinal cord - can improve over time.
  3. Brown-Sequard syndrome - damage to the R side of the spinal cord results in loss of voluntary motor control on the R side and loss of pain and temperature sensation on the left.
  4. ACS - loss of motor, pain, and temperature sensation. Preservation of touch and proprioception.
  5. PCS - loss of position, vibration, and touch sense with preservation of motor, pain and temperature.
57
Q

Central Cord Syndrome

A

Incomplete injury of spinal cord - Can improve over time.

58
Q

Brown-Sequard Syndrome

A

Incomplete spinal cord injury that results in loss of motor control on the damaged side and loss of sensation on the undamaged side.

59
Q

Anterior Cord Syndrome

A

Incomplete spinal cord injury - results in loss of motor, pain, and temperature. Proprioception and touch remain.

60
Q

Posterior Cord Syndrome

A

Incomplete spinal cord injury - results in loss of proprioception and touch. Motor, pain, and temp remain.

61
Q

Conus medullaris syndrome

A

Damage to the lumbar roots - severe back pain. Saddle anesthesia. Loss of bladder/bowel reflex. Lower limb paresthesia and possible paralysis.

62
Q

Acute complications of spinal cord injury
1. Timeframe
2. Cause?
3. Symptoms?

A
  1. Occurs immediately or within hours of injury
  2. Cause- the injury terminates impulses from higher brain
  3. Symptoms - massive vasodilation (decreased SV, HR, and BP) this is due to loss of innervation from the SNS.
    Loss of motor, sensory, reflex, and autonomic activity below the level of injury due to loss of innervation
63
Q

What is neurogenic shock?

A

A form of distributive shock that occurs in severe cervical and upper thoracic injury. Loss of sympathetic tone due to loss of innervation leads to vasodilation, bradycardia, hypotension.

More severe than spinal shock.

64
Q

What causes orthostatic hypotension in the context of SCI?

A

Vasoconstriction message from the medulla cannot reach blood vessels due to SCI.

65
Q

What is autonomic dysreflexia?
- Patho
- Cause
- Symptoms
- Treatment

A

A longer-term manifestation of SCI, usually months later. Medical emergency - can result in death. Noxious stimuli located below the level of the SCI sets off a sympathetic response. Commonly associated with bladder distention, pressure ulcers.

SNS increases the HR, vasoconstricts and does all its normal functions to get ready for fight or flight. The problem is the parasympathetic nervous system which would normally offset these changes is unable to reach the area of the body below the SCI. This results in maintained vasoconstriction in the levels below the SCI, leading to dangerously high BP.

Symptoms:
- Headache (throbbing) - initial
- HTN
- Bradycardia
- Flushing and sweating above SCI, cool and clammy below SCI
- Blurred vision

Treatment:
- Elevate HOB
- Fix the offending stimulus (check catheter for kinks, check for bowel impaction, administer anti-hypertensives), turn patient to see under if something hurting them

66
Q

What is always assessed with any new patient?

A

New admission:
1. CC
2. HPI
3. PMH
4. FMH
5. Personal and social history

67
Q

What changes in admission exams will be done for patients with suspected disorders of motor and brain function?

A
  1. Assessment of mental status
  2. GCS - if brain injury is suspected
  3. Mini-mental exam (commonly used for dementia)
68
Q

What is increased intracranial pressure? How can it affect the neurologic system?
What is the cranial cavity composed of?
What is a normal ICP?

A

Increased ICP is higher pressure in the cranium. These higher levels of pressure can push on the delicate components of the brain. The brain cannot stretch to compensate the increased pressure.
1. Interrupt blood flow
2. Destroy brain cells
3. Displace brain tissue (shift or mass effect)

The cranial cavity is composed of 10% blood, 10% CSF, and 80% brain.

A normal ICP is 0-15 mmHg

69
Q

Monro-Kellie Hypothesis

A

Shifting of brain contents to compensate for increased ICP

70
Q

Vasogenic edema

A

A type of cerebral edema that involves impairment of the blood-brain barrier allowing water and protein to shift from the vasculature into the interstitial space.

71
Q

Primary (Direct) injuries

A

Damage is caused by impact.
Focal-contusion, laceration, hemorrhage.
Diffuse concussion, shearing injuries, diffuse axonal injuries.

72
Q

Secondary brain injury

A

Caused by brain swelling, infection, and cerebral hypoxia.

73
Q

Coup-Countercoup

A

Accelerate/Decelerate injury

The brain floats freely in CSF in the skull. Rapid changes in speed can cause the brain to smash into the front of the skull (impact) and then the back of the skull (recoil).

74
Q

Post concussion Syndrome
1. What is a concussion?
2. Recovery
3. What symptoms can stick around after a concussion? How long?

A
  1. Immediate and transient loss of consciousness can be accompanied by a period of amnesia.
  2. Within 24 hours
  3. Headache, irritability, poor concentration and memory, and insomnia can stick around months afterwards.
75
Q

How does the brain get blood flow?

A

Bilateral cerebral arteries are the primary suppliers. Vertebral arteries are located posteriorly. Both of these tracts connect at The Circle of Willis provides a redundant flow of blood to the brain structures.

76
Q

How is cerebral blood flow regulated? Provide examples.

A
  1. Autoregulation-
    The body will largely autoregulate its blood supply to the brain. Any narrowing of arteries can lead to collateral formation or increased BP to attempt to overcome the narrowing.
  2. Sympathetic stimulation
    When the body detects dangerous situations, such as with reduced blood flow, it will release norepinephrine and epinephrine which stimulate an increase in HR, vasoconstriction, RAAS all which work to increase the blood pressure and improve cerebral blood flow.
  3. Metabolic -
    CO2 - vasodilator
    Hydrogen
    Oxygen levels - regulates vasoconstriction
77
Q

Subdural Hematomas
1. Types
2. What vessels
3. Where

A
  1. Can be acute or chronic (slow bleed)
  2. Small veins
  3. Between the dura and the arachnoid space (below the dura)
78
Q

Epidural hematomas
1. Type of injury associated with?
2. Where

A

Most commonly seen with skull fractures. More commonly seen in arterial damage.

Develops between the inner table of the bones of the skull and dura. Above the dura.

79
Q

Subarachnoid hemorrhage

A

Characterized by having a thunderclap headache - worst headache they have ever felt.

Occur in the setting of a ruptured cerebral aneurysm or arteriovenous malformations.

80
Q

Two main types of strokes
1. Which is most common
2. Common causes

A

Ischemic stroke - most common - commonly caused by interruption of blood flow to the cerebral vessels. Account for 70-80% of all strokes. TPA within 3 hours to break up the blockage and restore blood flow.

Hemorrhagic stroke - bleeding into the brain tissue. Seen with hypertension, aneurysms, arteriovenous malformations, head injury, or blood dyscrasias, falling while on blood thinners.

81
Q

What increases the risk for strokes?

A

HTN, smoking, DM, family history, carotid stenosis, sickle cell disease, HLD, AFIB

82
Q

What deficits are related to strokes?

A

Motor changes
Dysarthria - slurred speech
Aphasia - expressive vs receptive

83
Q

Cerebral Aneurysms
1. What is an aneurysm?
2. Symptoms?
3. Treatment?

A
  1. Outward bulging of the blood vessels of the brain.
  2. Depends on the size of the aneurysm. Small ones are typically asymptomatic. Larger ones can cause chronic headaches, neurologic deficits. If larger enough it can increase ICP leading to related symptoms.
  3. Depends on the location of the aneurysms -
84
Q

What does the pituitary gland do?

A

Releases hormones.
F - FSH
L - LH
A - ACTH
T - TSH

P - prolactin
I -
G -growth hormone

85
Q

What type of brain bleed is associated with aneurysms? What increases the risk for this type of bleed?

A

Subarachnoid hemorrhage.

Increased ICP. HTN. Smoking. Excessive alcohol intake.

86
Q

What happens at arteriovenous malformations? Why do they increase the risk for brain bleeds?

A

Blood is shunted from the higher-pressure arterial system to the lower pressure venous system without the filtering benefit of the capillaries. It also reduces tissue perfusion as the high-pressure blood is pushed away from the surrounding tissues.

The venous system is not used to these higher pressures and are more likely to rupture and hemorrhage under the increased strain.

87
Q

Broca’s aphasia

A

Expressive aphasia - trouble formulating speech

88
Q

Wernicke aphasia

A

difficulty understanding written or spoken language

89
Q

What part of the brain is affected by encephalitis

A

Parenchyma

90
Q

Meningitis
1. What is affected?
2. Symptoms?
3. Causes?
4. Assessments?

A
  1. Inflammation of the pia mater, the arachnoid. and the CSF- filled subarachnoid space.
  2. Fever, chills. Headache. Stiff neck, back, abdominal. N/V.
  3. Can be caused by viral or bacterial pathogens
  4. Brudzinki’s, Kernigs, nuchal rigidity
91
Q

Encephalitis
1. What is affected?
2. Causes?
3. Progression

A
  1. Inflammation of the brain parenchyma.
  2. Viral (herpes, west Nile), bacterial, fungi
  3. Can develop necrotizing hemorrhage at the site of the infection. Degeneration of the nerve body cells. Edema.
92
Q

Epilepsy

A

Reoccurring seizures.

93
Q

Focal seizures

A

A specific area in the body is affected

94
Q

Absent seizure

A

Staring off, disassociating while the seizure persists.

95
Q

Atonic seizure

A

Flaccid seizure (no movement)

96
Q

Myoclonic seizure

A

Stereotypical seizure with jerking movements

97
Q

Tonic seizures

A

Sudden muscle stiffness

98
Q

Tonic-clonic seizure

A

AKA grand mal

Loss of consciousness and jerking movements

99
Q

Status Epilepticus

A

Uncontrolled continuous seizure activity. Worried about the patient’s airway. Secure the airway and treat the seizures.

100
Q

Describe the pathophysiology behind Myasthenia Gravis
What organ is often considered when discussing etiology?

A

MG is a result of autoimmune destruction of the Ach receptors located on the muscles side of the neuromuscular junction.

The thymus is often pointed to as a cause of this acquired autoimmune disorder.

101
Q

What body systems/parts are particularly affected by MG? Why?

A

The eyes, speech/swallowing (bulbar), limbs, and respiratory muscles.
These muscles require constant motion, using up the limited supply of Ach quickly, resulting in weakness.

102
Q

How does MG present throughout the day?

A

MG worsens as the day goes on, muscle contraction and movement, even if just passive, will deplete the Ach stores resulting in weakness.

103
Q

What two methods does MG lead to a dysfunction of Ach

A
  1. Antibodies are formed, typically associated with the thymus, and attack Ach receptors at the neuromuscular junction.
  2. Antibodies form and attack the MUSK receptors at the neuromuscular junction. These receptors are responsible for Ach production.
104
Q

What ocular issues can be seen with MG?

A

Ptosis
Diplopia

Muscle weakness

105
Q

MG crisis
1. Why is it emergent?

A

Associated with ventilatory weakness and difficulty controlling secretions

106
Q

Endrophonium / Tensilon test

A

Classic method of diagnosing MG. This medication is a short acting Ach inhibitor leading to rapid improvement

107
Q

What part of the body does MS affect? How does it alter this part?

A

MS is a chronic demyelinating disease affecting the CNS. Results in loss of the myelin sheath (white matter). These sheaths play a pivotal role in the nervous system by protecting, nourishing, and speeding up neurons.

108
Q

How does MS progress as a disease? What causes this type of presentation?

A

MS is a chronic progressive disease that has periods of relapsing and remitting symptoms. This type of presentation is due to periods of myelin destruction followed by periods of remyelination.

109
Q

What are the plaques seen in MS?

A

The plaques are formation of scar tissue along axons. This further slows down the neurons electrical impulses.

110
Q

What signs and symptoms are seen with MS?

A
  1. Motor deficits: weakness, spasticity, tremors
  2. Sensory disturbance: paresthesia, hypoesthesia
  3. Bulbar dysfunction
  4. Vision disturbances

Advanced Pathophysiology (12 decks)

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