Disorders of Neural Function

Cluster headaches Clinical manifestations and occurance

´Occur in clusters up to 8 times/day lasting minutes to hours for a period of days to months followed by a long period of remission

´Most commonly occurring men between 20 to 50 years old

´Unilateral manifestations which can alternate sides with each headache

´rapid onset of severe, stabbing and throbbing pain around the eye

´eye redness, tearing

´eyelid edema

´drooping eyelid (ptosis)

´excessive pupil constriction (miosis)

´stuffy, runny nose

What is a migraine, it’s etiology, occurance, and clinical manifestations

´Episodic disorder characterized by headache lasting 4 to 72 hours

´Most commonly occurring in women 25 to 55 years old

´Caused by combination of multiple genetic and environmental factors

Clinical manifestations:

´Unilateral, throbbing, worsened by movement,

    moderate or severe, and one of the following:

´nausea and/or vomiting,

´photophobia (intolerance of light)

´phonophobia (fear of loud sounds)

´visual disturbances

´with or without an aura

What is a tension headache, occurance, and clinical manifestations

´Most common recurrent headache

´Average onset 20-30 years of age

´Mild to moderate bilateral headache with sensation of a tight band or pressure around the head with gradual onset of pain

´Occurs in episodes and may last for several hours or several days

´Not associated w/ nausea, vomiting or worsened by activity

what areas do they occur? (Slide)

What is the normal range temperate?

Normal range: 97°F – 99.5°F

Thermoregulation maintained through:

´Heat production

´Heat conservation

´Heat loss

how does thermoregulation vary in response?

´Activity

´Environment

´Circadian rhythm

´Gender

Mechanisms of Heat Loss

Radiation – transfer of heat through air

Conduction – transfer of heat between two touching objects

Convection – transfer of heat through circulation of air currents

Evaporation – transfer of heat through evaporation of water

what alteration is this? Elevation in core temperature above a 'set-point' that is normally regulated by the thermoregulatory center in the hypothalamus

Fever(Pyrexia)

(pathogenesis?) of fever(pyrexia)

´usually associated with an inflammatory response  

´pyrogenic cytokines that act on the hypothalamus to ↑ production of

     prostaglandin E2 which causes an ↑ in the ‘set point’

What are the manifestations of Fever? (Think what will come first and how will body cool tenmperature down)

•sweating

•chills and shivering.

•headache.

•muscle aches (myalgia)

•joint aches (arthralgia)

•↑ respiratory and heart rates

•loss of appetite (anorexia)

•dehydration

•general weakness

What is this alteration? Pathologic elevation of core temperature without an increase in the hypothalamic set point

Hyperthermia

Why does it occur? and what does progression look like?

Thermoregulatory center overwhelmed by:

•excess heat production

•impaired heat loss

•excessive environmental heat

Progression:

•heat cramps

•heat exhaustion

•heatstroke

What is this alteration? Core temperature of less then 95°F.

Usually related to exposure to cold environment

Hypothermia

Manifestations of Hypothermia?

Manifestations

•Shivering

•Slurred speech or mumbling

•Slow, shallow breathing

•Weak pulse

•Clumsiness or lack of coordination

•Drowsiness or very low energy

•Confusion or memory loss

•Loss of consciousness

1.Describe the etiology, pathogenesis, and clinical manifestations of disorders of motor function: muscular dystrophy, ( A group of inherited disorders recognized by progressive degenerative muscle weakness and loss of muscle tissue.) Most common type: Duchenne MD

occurs almost exclusively in males; X-linked recessive

Manifestations: (why do these occur)

•delayed developmental milestones

•delayed/loss of motor skills/poor coordination

•clumsiness/problems walking/frequent falls

•calf hypertrophy

•scoliosis or lordosis

Complications: (How does it develop into these)

•cardiomyopathy

•recurrent respiratory infections

•death r/t heart failure

1.Describe the etiology, pathogenesis, and clinical manifestations of disorders of motor function: myasthenia gravis, (Autoimmune disorder affecting the neuromuscular junction) Three times more common in females than males

Etiology: ´Acetylcholine receptors are impaired/destroyed leading to disrupted communication between the nerve and the muscle

Pathogenesis; ´Result in weakness of the voluntary skeletal muscles

Clinical Manifestations:

•drooping of one or both eyelids (ptosis)

•blurred or double vision due to weakness of the muscles that control eye movements

•weakness in the neck, fingers, hands,

     arms and legs

•impaired speech

•difficulty swallowing

•shortness of breath

1.Describe the etiology, pathogenesis, and clinical manifestations of disorders of motor function: Guillain-Barré Syndrome: Loss of myelin, edema, and inflammation of the affected nerves causes a loss of neurotransmission to the periphery.

Cause: unknown; thought to be autoimmune triggered by a viral or bacterial infection (respiratory or GI)

Manifestations:

´bilateral ascending from feet to hands

    “toes to nose”

•paresthesia (tingling/numbness)

•muscle weakness & flaccid paralysis

•absent reflexes

•muscle cramps

1.Describe the etiology, pathogenesis, and clinical manifestations of disorders of motor function: Parkinson’s disease,Neurodegenerative disorder that affects predominately dopamine-producing neurons in a specific area of the brain called substantia nigra.

progress will result in ´results in a lack of dopamine

Causes:

´unknown

´genetic vulnerability activated by an environmental trigger (e.g. virus) is thought to be a strong possibility

Clinical Manifestations: stooped posture , rigidity , flexed elbows/wrists, masked facial expression, reduced arm swinging, slightly flexed hips and knees, trembling of extremities, shuffling and short stepped gait

1.Describe the etiology, pathogenesis, and clinical manifestations of disorders of motor function: , amyotrophic lateral sclerosis(ALS, Lou Gehrig disease)

A progressive degenerative disease that destroys the neurons that control voluntary muscles.

´Cause: unknown

´Patho:

•degeneration of upper & lower neurons

•resulting in paralysis

clinical manifestations-

Manifestations of upper motor neuron lesions include weakness, spasticity or stiffness, and impaired fine motor control.

Manifestations of Lower motor neuron lesions include fasciculations, weakness, muscle atrophy, and hyporeflexia.

Dysphagia, dysarthria, and dysphonia

1.Describe the etiology, pathogenesis, and clinical manifestations of disorders of motor function: , multiple sclerosis.

Immune-mediated inflammatory disease involving degeneration of the CNS myelin, scarring, and loss of axons.

´myelin is destroyed leaving multiple areas of scare tissue or sclerosis

´leading to impaired communication between nerve cells, and

´permanent loss of function

Risk factors:

• Common in Northern European ancestry,

• s more common in northern latitudes,

pathogenesis: immune-mediated disorder where immune response attacks the central nervous system proteins.

Clinical Manifestations;

• abnormal gait,

• bladder

• sexual dysfunction,

• vertigo,

• nystagmus,

• fatigue,

• speech disturbance.

If damage is done to the white matter

Depression, euphoria, inattentiveness, apathy, forgetfulness, and loss of memory

1.Explain the clinical manifestations and mechanisms of brain injury.

2.Discuss cerebrovascular disease including cerebral circulation, the pathologies of ischemic and hemorrhagic stroke, and clinical manifestations of stroke.

3.Discuss the causes, pathophysiology, and clinical manifestations of infections of the central nervous system: meningitis and encephalitis.

5.Describe the changes in brain tissue and clinical manifestations occurring with Alzheimer’s disease.

Manifestations of Brain Injury

Altered levels of consciousness

•full consciousness

•confusion

•lethargic

•obtunded

•stupor

•coma

Alzheimer Disease and pathophysiology , manifestations

Leading cause of severe cognitive dysfunction in older persons

Pathophysiology: degeneration and atrophy of brain tissue due to:

´extracellular beta-amyloid deposit (plaques)

´intracellular neurofibrillary tangles

Manifestations:

Mental:

•memory loss

•disorientation to place & time

•loss of facial recognition

Behavior - progressive impairment in:

•cognition

•language

•abstract thinking

•judgement

´

Neurocognitive Disorders (Dementia)

Overall term for decline in mental function severe enough to interfere with a person’s ability to perform usual daily activities

Caused by damage to or loss of nerve cells and their connections in the brain

•neuron degeneration

•brain tissue compression

•atherosclerosis

•brain trauma

•infection and neuroinflammation

•genetics

Manifestations

In normal cognitive aging, cognitive ability is still intact just slower where as this is more quicker

Focal seizures:

Originating in one area of the brain, the two types are simple focal and complex focal

´Simple focal seizures -

seizure begins in a specific (focal) area of the brain, but can become generalized and spread to other areas. These seizures can cause twitching, changes in sensation, such as a strange taste or smell, hallucinations, strong emotions (e.g. fear, anxiety, déjà vu)

´Complex focal seizures –

often preceded by simple focal seizure, stare blankly into space or experience automatisms)

Generalized Seizures

Abnormal neuronal activity on both sides of the brain. The 4 are absence seizures, tonic seizurws, tonic-clonic, status epilepticus.

´Tonic seizures –

cause stiffening of muscles of the body, generally the extremities.

Absence seizures (petit mal seizures)

can cause rapid blinking, a few seconds of staring into space and/or jerking or twitching muscles.

Tonic-clonic seizures, also called grand mal seizures,

•Cry out

•Lose consciousness

•Fall to the ground

•Have muscle jerks or spasms

•Phases:

otonic

oclonic

postictal

Status epilepticus •active part of tonic-clonic

lasts 5 min or longer

•having a 2^nd seizure without recovery from the 1^st  one

•repeated seizures for 30 min or longer