BIOL 2200 Module 8: Neurological Disorders

Consciousness

State of being aware of one’s self and the environment, plus being capable of orienting to new stimuli

Which two components is consciousness divided into?

Arousal (wakefulness) + content and cognition

Arousal (wakefulness)

State maintained by the reticular activating system (RAS)

Reticular Activating System (RAS)

Diffuse network involving the brainstem and a functioning cerebra cortex

What does a loss of arousal indicate?

It indicates injury to the RAS or to both cerebral hemispheres

Does injury to one cerebral hemisphere typically lead to loss of arousal?

Injury to one cerebral hemisphere typically does not lead to loss of arousal

Selective attention

The ability to selectively process certain information

Executive attention

The ability to sustain attention, remember instructions, and possess self-control

Coma

Unarousable state

Stupor

State only arousable to pain

Obtundation

“Sleepy” state

Delirium

State of restlessness, hallucinations, and delusions

Glasgow Coma Scale

A scale that scores patients based on eye opening, verbal response, and motor response to indicate their LOC

Is a Glasgow Coma Scale score of 0 possible?

A score of 0 is NOT possible!

Brain death

State where no recovery is possible, and the brain cannot maintain homeostasis. No motor reflexes, cannot breath properly, lack of other causes (e.g. shock)

Cerebral death

Irreversible coma where brain stem may maintain homeostasis

Persistent vegetative state

Unawareness of self or surrounding environment, BUT sleep-wake cycles and brain stem reflexes are intact

Minimally conscious state

State where individuals can follow simple commands and gesture

Locked-in syndrome

Full paralysis of voluntary muscles EXCEPT eye movement

Cheyne-stokes breathing

Result of higher brain injury, characterized by periods of apnea and tachypnea, in response to levels of carbon dioxide in blood (irregular breathing pattern)

Neurogenic hyperventilation

>40 breaths/minute from midbrain injury where inspiratory/expiratory centers are continuously stimulated

How do pupils appear in severe hypoxia?

They appear dilated and fixed

What does damage/pressure to one oculomotor nerve cause?

A “blown” or non-responsibe pupil

Oculocephalic reflex

Movement opposite from head movement. Abnormal if eyes follow head movement or move independently (only assessable in comatose patients)

Decorticate posture

Posturing where upper extremities are flexed at elbows and lower extremities are rotated inwards and extended (gasp)

What typically causes decorticate posture?

Severe cerebral hemisphere damage

Decerebrate posture

Increased tone in certain muscles, clenched jaw, extended neck. All four limbs rigidly extended

What typically causes decorticate posture?

Brain stem lesions

Seizure disorder

A sudden, extreme, and abnormal discharge of cerebral neurons causing a temporary change in brain function. E.g. uncontrollable convulsions

Focal seizure

Seizure beginning at one side of the brain

Generalized seizure

Seizures involving both sides of the brain

Staring spells

Generalized seizure where the body does not shake. Often goes unnoticed

Agnosia

Inability to recognize form/nature of objects. Typically only affects one sense

Hemineglect

Inability to react to stimuli coming from the opposite side of damage. Will not orient or reach to neglected side

Dysphasia

Inability/insufficient ability to understand words or symbols. From dysfunction in left cerebral hemisphere

Aphasia

Inability to communicate. Interchangeable with dysphasia

Broca’s aphasia

Damage to brain area responsible for language production (speaking)

Wernicke’s aphasia

Damage to brain area responsible for language comprehension (understanding)

Common causes of Increased Intracranial Pressure (ICP)

Tumors, edema, hemorrhage

Monro-Kellie hypothesis

Hypothesis stating that increased intracranial pressure is compensated by reduction in other cranial contents. E.g. blood volume or CSF

Stage 1 of intracranial hypertension

CSF is displaced into spinal subarachnoid space → Compression of venous system

Stage 2 of intracranial hypertension

Swelling increases in ICP → decrease in brain tissue perfusion → hypoxemia → confusion * Cushing’s reflex

Cushing’s reflex

Systemic vasoconstriction in response to overcome decreased flow in the brain. Associated with intracranial hypertension

Effects of Cushing’s reflex on BP, HR, RR

BP → increases

HR & RR → decreases

Stage 3 of intracranial hypertension

Cerebral perfusion pressure falls → hypoxia and hypercapnia of brain tissue → deterioration in functions

Stage 4 of intracranial hypertension

Brain tissue herniates 9shifts) from the compartment of higher pressure to a compartment of lower pressure. ICP equals systolic arterial pressure

Consequence of ICP equalling systolic arterial pressure

Cerebral blood flow ceases, causing death

Brain herniation

Where increased pressure pushes brain tissue out of its normal position. Such as from ICP

Cerebral edema

Increased fluid content causing increased brain tissue volume

Vasogenic edema

Where increased blood-brain-barrier permeability leads to leak of plasma proteins and increased tissue water content

Which brain matter does vasogenic edema typically occur in?

White matter

Which brain matter does cytotoxic edema typically occur in?

Grey matter

Hydrocephalus

Excess fluid in ventricles and/or subarachnoid space. Caused by excess CSF or little CSF reabsorption

Noncommunicating hydrocephalus

Where obstruction (inflammation) prevents CSF from reaching arachnoid villi and being reabsorbed

Communicating hydrocephaluw

Failure of CSF reabsorption from reduced or scarred arachnoid villi from meningitis.

• Also overproduction of CSF by adenomas of choroid plexus

Muscle tone

Normal muscle tension that enables controlled movement