Flashcards in Neurology Pathophysiology Deck (29):
Peripheral Nervous system can be broke down into which divisions?
CNS is made up of what?
PNS can be broken down into the Sensory(afferent) division and the Motor (Efferent) division.
The motor division is then divided into the Autonomic Nervous System and the Somatic Nervous system.
Autonomic NS is further divided into the sympathetic and parasympathetic divisions.
CNS is made up of the brain and spinal cord. Encased in bone.
Describe embryonic development of the brain and spinal cord.
1. Neural plate forms from surface of ectoderm.
2. neural plate invaginates forming the neural groove flanked by the neural folds.
3. Neural fold cells migrate to form the neural crest, which forms much of the PNS.
4.leading to neural tube?
What is responsible for the development of the CNS? nerves of the PNS?
neural crest responsible for nerve of the PNS
WHat are the nervous system cell types?
Astorcytes: connective tissue cells
Microglia: act as mfs
Ependymal cells: line cavities, cuboidal or columnar cells, they absorb fluid across spinal cord.
Oligodendrocytes: surround nerve fibers and act in the brain as the schwann cells do in the periphery. Form myelin sheath.
-describe charge and solutes inside and outside of axon.
-describe an AP
-are AP summative?
-describe potential conduction velocity
-where do APs occur in myelinated and unmyelinated neurons?
-Inside: K+, negatively charged
-Outside: positively charged, Na+
-all or none events
-influx of Na+ into cell leads to depolarization, once this peaks K+ channels open and K+ leaves, repolarizing the cell.
No, AP are not summative.
Conduction velocity: depends upon fiber diameter and whether or not the axon is myelinated or not. Larger myelinated fibers conduct faster than smaller unmyelinated fibers.
APs occur at the nodes of Ranvier in myelinated axons, and occur subquentially one right after another the entire length of the axon in unmyelinated axons.
What are the 5 lobes of the brain and function of each?
Frontal: "secretary", primary motor cortex, brocas area(speaking and writing), solving complex multitask problems, personality, judgement.
Temporal: understanding language (wernickes; comprehension and speech), memory, hearing, sequencing and organization.
Occipital: interprets color light and movement
Parietal: sense of touch, pain, temp (sensory cortex), Spacial and visual perception
Insula; deep within the lateral sulcus, conciousness, emotion, self-awareness, interpersonal experience.
Edema in the CNS:
-how might this occur?
-why is this a special problem in the brain and spinal cord?
How: increase in tissue mass that results from the excess movement of body fluid from the vascular compartment or its abnormal retention in the tissue.
-lack of lymphatics
-lack of anastomoses in venous drainage
What is Vasogenic Edema?
Vasogenic: occurs when the blood brain barrier is upset either d/t inflammation from infection, toxic agents that damage capillary endothelium, abnormal capillaries associated with malignant neoplasm....these all cause leakage of proteins and fluid into the interstitium leading to swelling!!!!
Cytotoxic: intracellular phenomenon, cells themselves are damaged d/t
-hypoxia; cardiac arrest, near drowning, strangulation, focal edema d/t blockage of an end artery.
-Toxic substances that impair Na/K+ pump, impair production of ATP
these lead to intracellular edema.
Cytotoxicity: give IV bolus of hypertonic solution such as mannitol to draw water into the vasculature and out of the brain.
* DO NOT DO THIS IN VASOGENIC SHOCK!!! it would further draw MORE fluid into the interstital space and INCREASE SWELLING!
Increased Intracranial pressure
Causes: tumor growth, edema, excess cerebrospinal fluid blockage, hemorrhage
Clinical Hallmarks of Increased Intracranial Pressure, can you do LP on these patients?
No, cannot do LP unless you want to herniate their brain and kill them.
When intracranial pressure is high, cerebral blood volume is altered in 4 stages...what are these?
1. vasoconstriction and external compression of venous system; few sx
2. increased intracranial pressure causes a decrease of O2 to neural tissue causing systemic vasoconstriction 3.; episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes (hypoventillation)
3. when ICP begins to =arterial pressure there is lack of compensation- beginning decompensation; hypoxia and hypercapneia leading to cytotxic edema, decreased level of arousal, widened pulse pressure, cheynes-Stokes respirations (abnormal breathing pattern characterized by progressively deeper and sometimes faster breathing, followed by apnea), bradycardia, pupils small and sluggish, *surgical or medical intervention needed*
4. All compensatory mechanisms have been exhausted, dramatic rise in ICP in a short time, autoregulation is lost causing vasodilation and further increasing intracranial volume, decreased cerebral perfusion leading to severe hypoxia and acidosis, brain contents herniate from area of high pressure to lower pressure, small hemorrhages develop, ipsilateral pupil dilation and fixation, progressing to bilateral fixed and dilated pupils
What happens when mean systolic arterial pressure equals ICP?
cerebral blood flow ceases
Which cerebral artery often becomes obstructed and causes strokes?
-lenticulostriate arteries which branch off of the middle cerebral artery stem.
Which arteries supply the medial and lateral parts of the cerebrum?
Medial: anterior cerebral artery
Lateral: Middle cerebral artery
Functions of Blood brain barrier?
-reduce number of infection s
-protect from circulating amino acids that might act as Neurotransmitters
-is selectively permeable to certain drugs and abx
What cells make up the blood brain barrier?
-Astrocyte foot processes
-blood capillary endothelial cells w/ tight junctions
The hand and face have the most representation on the cortex, this is the area with the greatest propensity of muscles for fine muscle movement. The rest of the body is not well represented, T/f?
Corona radiata becomes more compacted and forms the internal capsule so if you have a stroke or lesion on the surface of the brain its going to involve less motor abnormality than if you have a lesion in the internal capsule, by the time the fibers get to the internal capsuel they are all squished together. Here a small lesion is going to cause a large deficit whereas a small lesion on the surface may not cause as large of a deficit. Once fibers get to the medulla there is decussation, any abnormality within the internal capsule is manifested on the opposite side of the individual. Right sided internal capsular lesion will manifest with left sided paralysis.
Cauda Equina begins at what level? Where do you do LP?
What makes up the white and gray matter of the spinal column?
Describe the route of nerve impulse as it approaches and leaves the spine.
WHite: nerve axons/myelin sheath
Gray: cell bodies
Dorsal root ganglion carries sensory info to the dorsal horn where it meets up with various interneurons that synapse and go to the other areas within the same segments or within the brain itself. The motor neurons exit through the ventral root and go to the muscles/target organ.
What are the three somatic sensations?
Mechanoreceptive (tactile, position/proprioceptive)
What do each of the following receptors sense?
-Free nerve endings
Free Nerve Endings: pain
Pacinian: pressure and vibration
Meissners:tactile, have highest sensitivity to light touch
What maintains balance?
Dorsal column, cerebellum, vision, ear
What are the two types of pain fibers? describe them.
A-delta fibers: fast sharp pain fibers (neo-spinothalamic tract), goes to somatosensory area
C-fibers: slow, dull, chronic pain fibers (paleo-spinothalamic tract), goes to intralaminar nuclei
What are the three levels of reflex pathways?
Lowest: spinal cord
Highest: cerebellum and basal nuclei
What are some signs of Upper Motor Neuron Lesions? Lower motor lesions?
Upper Motor Neuron:
-paralysis or weakness of movements of the affected side but gross movements may be produced.
-Babinskis sign present
-Loss of performance of fine-skilled voluntary movement
-Superficial abdominal reflexes and cremasteric reflex absent
-Spasticity of muscles
-Exaggerated DTR and clonus
Lower Motor Neuron:
-flaccid paralysis of muscles
-atrophy of muscles supplied
-loss of reflexes
-muscle fasciculations(spontaneous contraction involving small groups of muscle fibers)
-Muscle fibrillation (rapid irregular unsychronized contraction)
-Presence of muscle wasting
WHat neurotransmitters are used in the sympathetic and parasympathetic neurons?
Sympathetic: Ach and NE/E