Term
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Definition
controls emotions, judgments, controls motor aspects of speech, primary motor
cortex for voluntary muscle activation |
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Term
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Definition
receives fibers with sensory information about touch, proprioception, temperature,
and pain from the other side of the body |
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Term
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Definition
| responsible for auditory information, and language comprehension |
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Term
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Definition
| center for visual information |
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Term
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Definition
| coordination of muscle function |
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Term
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Definition
(midbrain, pons, and medulla)-respiratory and cardiac center, nerve pathways to the
brain |
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Term
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Definition
| (thalamus, subthalamus, and hypothalamus) |
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Term
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Definition
Integrate and relay sensory information from the face, retina, cochlea, and taste
receptors. (Interprets sensation of touch, pain and temperature). |
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Term
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Definition
1. Controls the autonomic nervous system and the neuroendocrine systems.
2. Maintains body homeostasis
3. Helps regulate body temperature
4. Helps regulate appetite control
5. Thirst Center
6. Sleeping Cycle
7. Control of Hormone secretion |
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Term
Autonomic Nervous System
Sympathetic (Fight or Flight): |
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Definition
1. Dilated pupils
2. Elevates heart rate and respiratory rate
3. Sweating
4. Epinephrine and norepinephrine secreted
5. Increased blood pressure
6. Constriction of skin and abdominal arterioles |
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Term
Autonomic Nervous System
Parasympathetic: |
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Definition
1. Constricted pupils
2. Lowers heart rate and respiratory rate
3. Increased peristalsis
4. Acetylcholine secreted
5. Decreases blood pressure
6. Relaxation of skin and abdominal arterioles |
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Term
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Definition
I-Olfactory-Smell
II-Optic-Vision acuity
III-Oculomotor – Eye function
IV-Trochlear – Eye function
V-Trigeminal – Sensory of the face,chewing
VI-Abducens – Eye function
VII-Facial – Facial expression, wrinkle forehead, taste anterior tongue
VIII-Vestibulocochlear – Auditory acuity, balance and postural responses
IX-Glossopharyngeal – taste on posterior 33% of the scale
X-Vagus – Cardiac, respiratory reflexes
XI-Spinal Accessory - Strength of trapezius and Sternocleidomastoid muscles
XII-Hypoglossal – Motor function of the tongue |
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Term
| Circle of Willis Arteries |
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Definition
1. Lateral striate
2. PCA- posterior communicating artery
3. Anterior communicating artery
4. MCA -middle cerebral artery
5. Anterior cerebral artery |
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Term
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Definition
lower extremity more involved than upper extremity, contralateral
hemiparesis and sensory deficits |
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Term
| Posterior cerebral stroke |
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Definition
| contralateral sensory loss, transient contralateral hemiparesis |
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Term
| Middle cerebral artery stroke |
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Definition
upper extremity more involved than the lower extremity,
contralateral sensory loss |
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Term
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Definition
1. Diabetes
2. Atherosclerosis
3. Hypertension
4. Cardiac disease
5. Transient ischemic attacks |
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Term
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Definition
Sympathetic innervation to the face is interrupted by a lesion in the brain
stem resulting in pupillary constriction, dry and red face with no sweat, ptosis-Mueller’s muscle,
problem located in sympathetic ascending fibers |
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Term
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Definition
caused by a lesion in the high thoracic or cervical cord. Severe
hypertension, sweating and headaches noted. May occur with a blockage in a urine catheter
Signs/Symptoms
1. Bradycardia
2. Headache
3. Increased parasympathetic activity
4. Excessive perspiration
5. Excessive sympathetic response
6. Elevated blood pressure
7. Stimulation of baroreceptors in aortic arch and caroticd sinus |
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Term
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Definition
a degenerative disease with primary involvement of the basal ganglia;
characterized by the following:
Signs/Symptoms
1. Bradykinesia
2. Resting tremor
3. Impaired postural reflexes
4. Rigidity
5. Loss of inhibitory dopamine
6. Mask like affect
7. Emotional lability |
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Term
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Definition
progressive demyelinating disease of the central nervous system affecting
mostly young adults
Cause unknown, most likely viral.
1. Fluctuating exacerbations
2. Demyelinating lesions limit neural transmission
3. Confirmed with lumbar puncture, elevated gamma globulin, CT/MRI, myelogram, EEG.
4. Mild to moderate impaired cognition common
5. Sensory Deficits
6. Bowel and Bladder Deficits
7. Spasticity common
8. Ataxic gait |
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Term
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Definition
neuromuscular disease characterized by fatigue of skeletal muscles and
muscular weakness.
**Key point-Review the differentiation between MG and a cholinergic crisis, using the Tensilon
Test. A cholinergic crisis may have hypotension, bradycardia vs. myasthenia gravis.
an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular junction,[1] inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated medically with cholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy.
Signs/Symptoms
1. Progressive involvement
2. Decreased muscle membrane acetylcholine receptors
3. Severe weakness (proximal more than distal muscles)
4. Facial, ocular and bulbar weakness
5. Possible life-threatening respiratory muscle weakness
6. Probable use of anticholinesterase drugs for treatment |
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Term
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Definition
an acute, autoimmune, polyradiculoneuropathy affecting the peripheral nervous system, usually triggered by an acute infectious process.
Signs/Symptoms
1. Demyelination of peripheral and cranial nerves
2. Motor paralysis in an ascending pattern
3. 3% Mortality – respiratory failure
4. Autonomic dysfunction-arrhythmias, blood pressure changes, tachycardia
usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment of plasmapheresis followed by immunoglobulins and supportive care, the majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and dysautonomia are present. |
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Term
| Amyotrophic lateral sclerosis (Lou Gehrig’s disease) |
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Definition
degenerative disease affecting upper and
lower motor neurons
Signs/Symptoms
1. Death typically in 2-5 yrs.
2. Spasticity, hyperreflexia
3. Dysarthria, Dysphagia
4. Autonomic Dysfunction in approximately 1/3 of patients
5. Cognition is normal |
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Term
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Definition
slowly progressive muscle weakness that occurs in patients with a history
of acute poliomyelitis, after a stable period
Sign/Symptoms
1. New Weakness
2. Pain/Myalgia
3. Abnormal fatigue
One theory of the mechanism behind the disorder is that it is due to "neural fatigue" from overworked neurons. The original polio infection generally results in the death of a substantial fraction of the motor neurons controlling skeletal muscles, and the theory is that the remaining neurons are thus overworked and eventually wear out.
Another theory holds that the original viral infection damages portions of the lower brain, possibly including the thalamus and hypothalamus. This somehow upsets the hormones that control muscle metabolism, and the result is a metabolic disorder similar to mitochondrial disorder that causes muscle pain and injury (via rhabdomyolysis) and also causes the fatigue. Some also believe that the original polio caused the atrophying of some muscles and as the person ages the weakness caused by loss of muscle mass due to aging is accelerated due to the person starting off with less muscle. Another possibility is that post-polio symptoms are due to some combination of mechanisms. |
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Term
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Definition
| recurrent seizures due to excessive and sudden discharge of cerebral cortical neurons. |
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Term
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Definition
In the tonic phase, the person will fall unconscious, and the person's muscles will suddenly tense up, often causing the extremities to either be pulled towards the body or rigidly pushed away from it, which will cause the person to fall to the ground if they are standing. The tonic phase is usually the shortest part of the seizure, usually lasting only a few seconds. The person may also express vocalizations sounding like a loud moan during the tonic stage, though this is not always the case.
In the clonic phase, the person's muscles will start to contract and relax rapidly, causing convulsions. These may range from exaggerated twitches of the arms and legs to violent shaking or vibrating of the stiffened extremities. The person may roll and stretch as the seizure spreads. The eyes typically roll back, the tongue is often bitten, and incontinence is seen in some cases. Post-ictal sleep invariably follows a tonic-clonic seizure. Confusion and amnesia upon awakening is usually experienced. |
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Term
| Absence seizures (Petit Mal) |
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Definition
| momentary lapses of consciousness. These seizures almost always begin in childhood or adolescence, and they tend to run in families, suggesting that they may be genetic. Some people with absence seizures have purposeless movements during their seizures, such as a jerking arm or rapidly blinking eyes. Others have no noticeable symptoms except for brief times when they are "out of it." Immediately after a seizure, the person can resume whatever he or she was doing. These seizures can happen a few times a day or in some cases hundreds of times a day to the point that the person cannot concentrate in school or other situations. Childhood absence epilepsy usually stops when the child reaches puberty. Absence seizures usually have no lasting effect on intelligence or other brain functions. |
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Term
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Definition
seizures which affect only a small region of the brain, often the temporal lobes and/or hippocampi. Simple partial seizures are often precursors to larger seizures
While awake some common symptoms of simple partial seizures are:
preserved consciousness
sudden and inexplainable feelings of fear, anger, sadness, or nausea
experience of unusual feelings or sensations
altered sense of hearing, smelling, tasting, seeing, and tactile perception (sensory illusions and/or hallucinations), or feeling as though the environment is not real or detachment from the environment (depersonalization)
deja vu (familiarity) or jamais vu (infamiliarity)
laboured speech or inability to speak at all
amnesia around the seizure event and sometimes events which occurred before the seizure
While asleep symptoms include:
onset usually in REM sleep
dream like state
appearance of full consciousness
hallucinations and/or delusions
behavior or visions typical in dreams
ability to engage with the environment and other people as in full consciousness, though often behaving abnormally, erratically, or failing to be coherent
complete amnesia or assimilating the memory as though it was a normal dream on regaining full consciousness |
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Term
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Definition
nvolves a greater degree of impairment or alteration of consciousness/awareness and memory than a simple partial seizure.
Complex partial seizures are often precipitated by an aura, which is itself a simple partial seizure. This may begin with a feeling of déjà vu or jamais vu. The person may then have feelings of fear, euphoria or depression, and possibly depersonalization. They may experience visual disturbances, such as tunnel vision or a change in the size of objects. Once consciousness is impaired, the person may display “automatisms” such as lip smacking, chewing, swallowing, and undressing oneself. There may also be loss of memory (amnesia) surrounding the seizure event. As the person may still be able to perform routine tasks such as walking or shopping, witnesses may not recognize anything is wrong.
Although the origins of complex partial seizure vary, they usually originate in the temporal lobes of the brain, particularly on the hippocampus. It is often caused by mesia lesions in the brain, which are essentially a ridge of scar-like tissue. Like more generalized epilepsy, complex partial seizures are caused by a misfiring of a synapse in the brain, which causes a “storm like” reaction with bursts of electricity that can result in changes in personality and physicality. Often, the abnormal activity spreads to the rest of the brain, causing a secondary generalized seizure. |
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Term
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Definition
inflammation of the meninges of the spinal cord and brain caused by bacteria.
The most common bacteria are the following: Neisseria meningitidis, Diplococcus pneumoniae,
and Haemophilus influenzae
Signs/Symptoms
1. Brudzinski’s sign
2. Kernig’s sign
3. Stiff/Tight neck
4. Fever
5. Confused |
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Term
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Definition
damage is mainly in anterior cord resulting in loss of motor function
and pain and temperature with preservation of light touch, proprioception and position sense |
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Term
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Definition
hemisection of SC resulting in ipsilateral weakness and loss of
position and vibration sense below the level of lesion |
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Term
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Definition
Vestibulospinal-conducts information from the vestibular labyrinth in the inner ear. It is responsible for adjusting posture to maintain balance.
Corticospinal- pyramidal tract is a massive collection of axons that travel between the cerebral cortex of the brain and the spinal cord. The major function of this pathway is fine voluntary motor control of the limbs. The pathway also controls voluntary body posture adjustments.
Rubrospinal- It is an alternative route for the mediation of voluntary movement. Involved in involuntary adjustment of arm position in response to balance information.
Corticobulbar- from the motor cortex to several nuclei in the pons and medulla. Involved in control of facial and jaw musculature, swallowing and tongue movements.
tectospinal tract/colliculospinal tract- nvolved in involuntary adjustment of head position in response to visual information. |
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Term
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Definition
Dorsal Column/Medial Leminiscal
Spinothalamic- pathway originating in the spinal cord that transmits information about pain, temperature, itch and crude touch to the thalamus.
Dorsal Spinocerebellar- conveys proprioceptive information from the body to the cerebellum.
Ventral Spinocerebellar - conveys proprioceptive information from the body to the cerebellum |
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Term
| Upper Motor Neuron Lesion |
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Definition
are motor neurons that originate in motor region of the cerebral cortex or the brain stem and carry motor information down to the final common pathway, that is, any motor neurons that are not directly responsible for stimulating the target muscle. The main effector neurons for voluntary movement lie within layer V of the primary motor cortex and are called Betz cells. The cell bodies of these neurons are some of the largest in the brain, approaching nearly 100μm in diameter.
These neurons connect the brain to the appropriate level in the spinal cord, from which point nerve signals continue to the muscles by means of the lower motor neurons.
A. Disuse atrophy
B. +Babinski
C. Hypertonia (Spasticity)
D. Weakness or paralysis of movement not individual muscles
E. Hyperreflexia |
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Term
| Lower Motor Neuron Lesion |
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Definition
LMNs are the motor neurons connecting the brainstem and spinal cord to muscle fibers, bringing the nerve impulses from the upper motor neurons out to the muscles. The lower motor neuron's axon goes through a foramen and terminates on an effector (muscle).
Damage to lower motor neurons (lower motor neurone lesions) is indicated by abnormal EMG potentials, fasciculations, paralysis, weakening of muscles, and neurogenic atrophy of skeletal muscle.
A. True Atrophy
B. Weakness of individual muscles
C. Fibrillations
D. Hyporeflexia |
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Term
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Definition
The typical pathway of a reflex may be outlined as follows: sensory receptor on dendrite of dorsal
root ganglion cell -------- ganglion cell ---------- axon cell -------- dorsal root -------- dorsal
horn of spinal cord-------- either directly to motor cell in ventral horn or via internuncial (
association) neuron to ventral horn motor cell------- axon via ventral root ------ spinal nerve-----
-- effector organ ( e.g., muscle). |
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