-No connection with the brain

-rapid response

-automatic

1.Stimulus.

2.Receptor fires AP if threshold is reached.

3.AP travels through sensory neuron.

4.Intergrating centre- diverging.

5.EFFERENT PATH 1: somatic motor neuron-effector 1 (quadricep muscle)- excitatory pathway, muscle contracts.

EFFERENT PATH 2: somatic motor neuron inhibited (by interneuron)- effector 2 (hamstring muscle)- inhibitory pathway, muscle stays relaxed. **Reciprocal Inhibition

ISCHEMIC STROKE

Blocked arteries- thrombotic/embolic.

·MCA: hemiplegia, loss of sensation, aphasia (if left hemisphere).

·ACA: sensory, motor and smell loss

·PCA: vission, memory, object recognition

Bleeding into brain or surrounding tissue- build up of pressure.

Aneurism//Angiomas (AVM)

- Glial cells: glioma -Metastasis

-Meninges: meningioma.

Encapsulated: defined entity.

Infiltrated: no clear 'boundaries' 

Rythmic electrical discharge.

CAUSES:

-Perinatal (anoxia) -Genetic -Toxins

-Tumours -Metabolic -Infections

-Prenatal

Recurrent seizures.

Diagnosis: EEG

GENERAL: Tonic phase- lose consciousness

Clonic phase- shaking

Post-ictal phase: unresponsive.

PETIT MAL: subtype of general seizure. 

NO electrical discharge.

FOCAL: begins in one place then spreads. Affects the part of the body related to the part of the brain involucrado.

TREATMENT: decrease membrane excitability by interfering with NTs.

-persistent -memory loss -2(+) cognitive disfunctions.

Causes: Neurodegenerative disorders (eg. alzheimer's)

Non-degenerative disorders (eg. toxins)

• Cognitive: memory loss, language (circumlocutory, empty, anomic-can't name objects)
• Behavioural: psychosis, leads to detereoration of normal social skills.
• No sensory/motor deficits

CORTICAL ATROPHY- neurofibrillary tangles, Amyloid plaques (build up of proteins, lowering WP of cells)

• Cognitive: executive dysfunction (frontal lobe)
• Behavioural: personality changes, socially innapropriate.
• No sensory/motor dysfunction.

CORTICAL ATROPHY

Hypokinetic: decreased blinking, facial expression, difficulty initiating movement, bradykinesia (extreme slowness)

Resting tremor: stops when movement is initiated.

Nigrostriatal Pathway

(Basal ganglia motor loop)

Normally, substantia nigra and association cortex (motor command) excite the striatum by releasing dopamine. 

The basal ganglia normally inhibits the thalamic relay so it cant excite the motor cortex (movement).

However, when the striatum is excited it inhibits the basal ganglia so the motor cortex is excited.

In Parkinson's, the substantia nigra is affected so less dopamine is released so the striatum can't inhibit the basal ganglia from inhibiting  the thalamic relay so less movement.