Mod 9

Question 1

General effects of neurological dysfunctions

Answer 1

a. manifestations of brain deterioration function
b. seizures
c. data processing deficits.
d. increase intracranial pressure.
e. alteration in neuromotor function

Question 2

Define consciousness. What two components?

Answer 2

It is the state of awareness of the self and the environment.

1. arousal.
2. content + cognition

Question 3

What parts of the brain are required for a normal state of arousal? What must be damaged to loss of arousal?

Answer 3

The RAS (reticular activating system) diffuse network involving brainstem medulla and thalamus, and the functioning CEREBRAL CORTEX. 
The loss of arousal is direct injury to the RAS or BOTH cerebral hemispheres (At the same time).

Question 4

What is included in “awareness”

Answer 4

Selective attention: ability to select specific information to process.

Memory: ability to store and retrieve information.

Executive attention: ability to maintain sustained attention, remember instructions and posses self-control.

Question 5

Describe levels of consciousness

Answer 5

Coma: none
Stupor: arousal, only to PAIN.
Obtundation: Low arousal, sleepy.
Delirium: restlessness, hallucination and and delusions
Confusions: fuzzy, disorientation, poor stimuli response

Question 6

Define brain death.

Answer 6

No recovery - homeostasis is lost and the brain cannot maintain function.

Question 7

How to determine brain death.

Answer 7

established pathology
unresponsive coma + absence of motor reflexes
absent brainstem reflexes
requires mechanical ventilation (apnea test)
lack of causes eg. drugs, shock

Question 8

Define/describe cerebral death

Answer 8

irreversible coma = brainstem can maintain homeostasis but they are unresponsive.

Question 9

Define/describe persistent vegetative state.

Answer 9

Complete awareness of self or the surrounding environment.

- sleep wake cycle are present, brain stem reflexes are intact, bowel and bladder incontinence.

Question 10

Define/describe minimally conscious state

Answer 10

May follow simple commands, manipulate objects, gesture and intelligble speech.

Question 11

Define/describe locked in syndrome.

Answer 11

Complete awareness - complete paralysis of voluntary muscles with the exception of eye movements.
fully conscious, cant communicate through speech or movement.

Question 12

Describe Cheyne-Stroke breathing and brain damage occurance.

Answer 12

Higher brain damage issue.
alternating periods of apnea and tachypnea, due to the response of CO2 in the blood.
- loss of smoothing out the breathing pattern usually performed by higher brain centers.

Question 13

Describe Neurogenic hyperventilation

Answer 13

Occurs in the midbrain

> 40 breaths per minute with inspiratory / expiratory centers are continously stimulated.

Question 14

What alterations. an occur with pupillary response and what information can this yield?

Answer 14

Pupillary changes – upon being exposed to light, pupil response can range from combinations of fixed, dilated, pinpoint, and unequal (pupils responses differ). Can help determine location/extent of brain damage.
For example: Severe hypoxia usually produces dilated, fixed pupils. Damage or pressure on the oculomotor nerve (cranial nerve III) to one eye will cause one pupil to be non- responsive (=“blown”).

Question 15

What is normal oculomotor “doll’s eye” response in a comatose patient? What are the two responses?

Answer 15

The oculocephalic reflex is movement opposite from head movement (doll’s eye response).
Abnormal is following head movement, or independent movement. (assessable only in comatose patients)

Question 16

Describe decorticate and decerebrate postures and location of brain damage they indicate.

Answer 16

Abnormal responses in the upper and lower extremities:
• Decorticate posture - upper extremities flexed at the elbows and held close to the body and lower extremities that are externally rotated and extended. May occur with severe cerebral hemisphere damage.
• Decerebrate posture – increased tone in extensor muscles and trunk muscles, with clenched jaw and extended neck = head in neutral position, all four limbs rigidly extended. Occurs with brain stem lesions.

Question 17

Define seizure. What are some causes of seizure?

Answer 17

Definition: a sudden, explosive, disorderly discharge of cerebral neurons, that produces a temporary change in brain function, usually involving motor, sensory, autonomic or psychic clinical manifestations and a temporary altered level of arousal.
Mild seizures may manifest as staring spells, no body shaking and may go unnoticed:
• Major seizures usually produce convulsions: jerky, muscle contraction - relaxation cycles
• Generally caused by cerebral lesions, biochemical disorders, cerebral trauma or epilepsy. (These factors can result from many causes, including fever, brain tumors, infections, genetic predispositions, etc.)

Question 18

What is the difference between a seizure and convulsion.

Answer 18

Seizure: sudden explosive discharge of cerebral neurons.

ConvulsionsL jerky, muscle contraction - relaxation cycles (can be caused by a seizure.

Question 19

Define Agnosia.

Answer 19

Agnosia – failure to recognize the form/nature of objects; usually only affects one sense (e.g., can recognize a safety pin by touching it, but not when looking at it). Caused by any damage to a specific part of the brain.

Question 20

Define Hemineglect

Answer 20

inability to attend to and react to stimuli coming from the contralateral (to site of damage) side of space. Won’t visually track, orient or reach to the neglected side. May not use those limbs, or take care of them.

Question 21

Define Dysphasia.

Answer 21

understanding (receptive) and use (expressive) of symbols (written or verbal) is disturbed or lost (e.g., cannot find words, or uses words, but meaningless). Caused by dysfunction in left cerebral hemisphere (stroke, cancer, trauma, etc.)

Question 22

Define Aphasia.

Answer 22

Aphasia literally means inability to communicate, but the term is used interchangeably with dysphasia:
– Broca’s aphasia: a result of damage to the centre of the brain responsible for the production of language.
– Wernike’s aphasia: a result of damage to the centre of the brain responsible for the comprehension of language

Question 23

What does IICP stand for and what does it mean? causes?

Answer 23

May result from anything that takes up volume in the brain, e.g., a tumour, edema, excess CSF or hemorrhage.
• To adjust for increased pressure, there must be a reduction in some other cranial content. This can include blood volume, CSF volume, tissue volume (Monro-Kellie hypothesis).
• The brain adjusts initially through loss of CSF, as it is most easily decreased in response to increased intracranial pressure.
• If this does not remedy pressure, cerebral blood volume and flow are altered.

Question 24

What 3 things can be adjusted to compensate for ICP changes? In what order?

Answer 24

Blood volume
CSF volume (1st)
Tissue volume

Question 25

Describe the 4 stages of IICP.

Answer 25

Stage 1: CSF is displaced into spinal subarachnoid space, and reabsorption increases. External compression of the venous system occurs in order to decrease the ICP (may be asymptomatic). (The blood is limited in how much it can buffer the increase in pressure, as increased levels of carbon dioxide in the brain tissue cause vasodilation. For this reason, hyperventilation is sometimes used to decrease ICP .) Stage 2 When continuing swelling exceeds this compensatory mechanism, further increases in volume produce significant increases in ICP. This results in a significant decrease in brain tissue perfusion, and oxygenation is compromised (resulting in confusion, restlessness, drowsiness). Neurons in the vasomotor center respond by causing systemic vasoconstriction. This results in increased systemic blood pressure, in order to overcome decreased flow in the brain (this is called “Cushing’s reflex”). Stage 3 With continued swelling, when ICP begins to equal mean arterial pressure in the body, cerebral perfusion pressure falls, and hypoxia and hypercapnia of brain tissue occur (rapid deterioration: decreased level of arousal, small, sluggish pupils). At this point, all compensatory mechanisms have been used, so there can now be a dramatic rise in ICP over a very short period of time. Stage 4: Brain tissue shifts (herniates) from the compartment of greater pressure to a compartment of lesser pressure. (Symptoms appear that depend upon which part of brain is affected.) This increases pressure in the lower pressure compartment, as well, impairing its blood supply. This increases ICP markedly to where it equals systolic arterial pressure, at which point cerebral blood flow ceases.

Question 26

Causes of IICP: Cerebral Edema (describe)

Answer 26

An increase in the fluid content, causing increase in brain tissue volume. • Occurs after trauma, infection, hemorrhage, tumour, ischemia, infarct or hypoxia. • Distorts blood vessels, displaces brain tissues, causes herniation. • Two types: 1. Vasogenic edema: increased permeability of BBB (plasma proteins leak out of capillaries, drawing water to them = increased water content of tissue. Occurs mainly in the white matter – easily separated fibers) 2. Cytotoxic edema: Toxins, hypoxia, etc. cause failure of transport mechanism of cells = more sodium inside cell = more water inside cell. Occurs mainly in the gray matter.

Question 27

Causes of IICP: Hydrocephalus

Answer 27

• Excess fluid in ventricles, subarachnoid space, or both • Caused by too high production, or too low reabsorption, of CSF • Two types: – Noncommunicating (obstructive): obstruction (tumour, inflammation, hemorrhage) prevents CSF from reaching arachnoid villi and being reabsorbed. – Communicating: failure of reabsorption due to too few, or scarring (due to meningitis) of arachnoid villi, etc. Adenomas of choroid plexus can also cause overproduction of CSF (much less common). • Signs and symptoms vary greatly, depending upon rapidity of onset (if acute onset -> IICP).

Question 28

What are the 3 alterations ghat can occur if the neuromotor function of the nervous system is affected?

Answer 28

Muscle tone is the normal state of muscle tension which allows for controlled movement and maintenance of posture. It is controlled by the stretch reflex,. • Alterations in muscle tone can be caused by injury to any section of motor pathway: peripheral nerve, neuromuscular junction, spinal cord, brain.

Question 29

What is muscle tone? How it controlled?

Answer 29

Muscle tone is the normal state of muscle tension which allows for controlled movement and maintenance of posture. It is controlled by the stretch reflex,. • Alterations in muscle tone can be caused by injury to any section of motor pathway: peripheral nerve, neuromuscular junction, spinal cord, brain.

Question 30

What changes in the muscle tone are brought by injuries to the upper motor neurons vs the lower motor neurons? include: hypotonia and hypertonia.

Answer 30

Symptoms depend upon where damage has occurred. An injury in the upper motor neurons (UMN) generally produces increased tone as the inhibitory effect of the brain on the spinal cord reflexes is removed (rigidity = hypertonia), while an injury in the LMN produces decreased tone (flaccidity = hypotonia).

Question 31

What are alterations in movement?

Answer 31

• Paresis/paralysis (1292) – – Paresis: weakness Paralysis: Loss of motor neuron function so that a muscle group is unable to overcome gravity • Can occur in both upper (brain and spinal cord) and lower (cranial/spinal nerves) motor neurons • For upper motor neuron (brain and spinal cord) – The condition can be classified as: hemiparesis/hemiplagia, paraparesis/paraplagia, quadriparesis/quadriplagia. • Hyperkinesia – Excessive movements (e.g., tremors, tics) – Due to physical or chemical causes (e.g., insufficient dopamine).

Question 32

Define hemi-, para-, quadra-

Answer 32

Hemi - vertical half Para - horizontal half Quadra - all 4

Question 33

describe the 3 alterations in complex motor performance

Answer 33

1. Disorders of posture An inequality of tone in muscle groups, because of a loss of normal postural reflexes. Already noted: decorticate and decerebrate postures. Also: basal ganglion posture (stooped, hyperflexed with narrow, short- stepped gait. 2. Disorders of gait E.g., spastic gait – a shuffling gait with leg extended and held stiff; scissor gait – stiff legs that swing around and cross in front 3. Disorders of expression E.g., Hypermimesis – inappropriate laughter or crying E.g., Dyspraxia/apraxia – inability performing tasks that require learned motor skills (speaking (dysarthria (1346)), writing (agraphia), using tools, following instructions). Problem is with use of muscles, not with comprehension.