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I!1[Jt!jfj Neurophysiology 53 D. Spinal organization of motor systems 1. Convergence occurs when a single a-motoneuron receives its input from many muscle spindle group Ia afferents in the homonymous muscle. produces spatial summation because although a single input would not bring the muscle to thr...
I!1[Jt!jfj Neurophysiology 53 D. Spinal organization of motor systems 1. Convergence occurs when a single a-motoneuron receives its input from many muscle spindle group Ia afferents in the homonymous muscle. produces spatial summation because although a single input would not bring the muscle to threshold, multiple inputs will. also can produce temporal summation when inputs arrive in rapid succession. z. Divergence occurs when the muscle spindle group Ia afferent fibers project to all of the a-motoneurons that innervate the homonymous muscle. 3. Recurrent inhibition (Ranshaw calls) Renshaw cells are inhibitory cells in the ventral hom of the spinal cord. They receive input from collateral axons of motoneurons and, when stimulated, negatively feedback (inhibit) on the motoneuron. E. Brain stem control of posture 1. Motor canters and pathways Pyramidal tracts (corticospinal and corticobulbar) pass through the medullary pyramids. All others are extrapyramidal tracts and originate primarily in the following structures of the brain stem: a. Rubrospinal tract originates in the red nucleus and projects to intemeurons in the lateral spinal cord. Stimulation of the red nucleus produces stimulation of flexors and inhibition of extensors. b. Pontine raticulospinal tract originates in the nuclei in the pons and projects to the ventromedial spinal cord. Stimulation has a general stimulatory affect on both extensors and flexors, with the predominant effect on extensors. c. Medullary reticulospinal tract originates in the medullary reticular formation and projects to spinal cord intemeurons in the intermediate gray area. Stimulation has a general inhibitory effect on both extensors and flexors, with the predominant effect on extensors. d. Lateral vestibulospinal tract originates in Deiters nucleus and projects to ipsilateral motoneurons and intemeurons. Stimulation causes a powerful stimulation of extensors and inhibition of flexors. a. Tectospinal tract originates in the superior colliculus and projects to the cervical spinal cord. is involved in the control of neck muscles. Z. Effects of transactions of the spinal cord a. Paraplegia is the loss of voluntary movements below the level of the lesion. results from interruption of the descending pathways from the motor centers in the brain stem and higher centers. b. Loss of conscious sensation below the level of the lesion c. Initial loss of reflexes----t~pinalshock Immediately after transection, there is loss of the excitatory influence from a- and y-motoneurons. Limbs become flaccid, and reflexes are absent. With time, partial recovery and return of reflexes (or even hyperreflexia) will occur. 54 BRS Physiology (1) If the lesion is at C7, there will be loss of sympathetic tone to the heart. As a result, heart rate and arterial pressure will decrease. (2) If the lesion is at C3, breathing will stop because the respiratory muscles have been disconnected from control centers in the brain stem. (3) If the lesion is at C1 (e.g., as a result of hanging), death occurs. 3. Effects of transactions above the spinal cord a. Lesions above the lateral vestibular nucleus cause decerebrate rigidity because of the removal of inhibition from higher centers, resulting in excitation of a- and y-motoneurons and rigid posture. b. Lesions above the pontine reticular formation but below the midbrain cause decerebrate rigidity because ofthe removal ofcentral inhibition from the pontine reticular formation, resulting in excitation of a- and y-motoneurons and rigid posture. c. Lesions above the red nucleus result in decorticate posturing and intact tonic neck reflexes. F. Cerebellum-central control of movement 1. Functions of the cerebellum a. Vestibulocerebellum-control of balance and eye movement. b. Pontocerebellum---planning and initiation of movement. c. Spinocerebellum-synergy, which is control of rate, force, range, and direction of movement. 2. Layers of the cerebellar cortex a. Granular layer is the innermost layer. contains granule cells, Golgi. type II cells, and glomeruli. In the glomeruli, axons of mossy fibers form synaptic connections on dendrites of granular and Golgi type II cells. b. Purkinie cell layer is the middle layer. contains Purkinje cells. Output is always inhibitory. c. Molecular layer is the outermost layer. contains stellate and basket cells, dendrites ofPurkinje and Golgi. type II cells, and parallel fibers (axons of granule cells). The parallel fibers synapse on dendrites of Purkinje cells, basket cells, stellate cells, and Golgi type II cells. 3. Connections in the cerebellar cortex a. Input to the cerebellar cortex (1) Climbingfibers originate from a single region of the medulla (inferior olive). make multiple synapses onto Purkinje cells, resulting in high-frequency bursts, or complex spikes. "condition'' the Purkinje cells. play a role in cerebellar motor learning. (2) Mossy fibers originate from many centers in the brain stem and spinal cord. include vestibulocerebellar, spinocerebellar, and pontocerebellar afferents. make multiple synapses on Purkinje fibers via interneurons. Synapses on Purkinje cells result in simple spikes. I!1[Jt!jfj Neurophysiology 55 synapse on granule cells in glomeruli. The axons of granule cells bifurcate and give rise to parallel cells. The parallel fibers excite multiple Purkinje cells as well as inhibitory interneurons {basket, stellate, Golgi type II). b. Output of the cerebellar cortex Purkinje cells are the only output of the cerebellar cortex. Output ofthe Purkinje cells is always inhibitory; the neurotransmitter is y-aminobutyric acid (GABA). The output projects to deep cerebellar nuclei and to the vestibular nucleus. This inhibitory output modulates the output of the cerebellum and regulates rate, range, and direction of movement (synergy). c. Clinical disorders of the cerebellum-ataxia result in lack of coordination, including delay in initiation of movement, poor execution of a sequence of movements, and inability to perform rapid alternating movements (dysdiadochokinesia). (1) Intention tremor occurs during attempts to perform voluntary movements. (2) Rebound phenomenon is the inability to stop a movement. G. Basal ganglia-control of movement 1. 2. 3. 4. consists of the striatum, globus pallidus, subthalamic nuclei, and substantia nigra. modulates thalamic outflow to the motor cortex to plan and executa smooth movements. Many synaptic connections are inhibitory and use GABA as their neurotransmitter. The striatum communicates with the thalamus and the cerebral cortex by two opposing pathways. Indirect pathway is, overall, inhibitory. Direct pathway is, overall, excitatory. Connections between the striatum and the substantia nigra use dopamine as their neurotransmitter. Dopamine is inhibitory on the indirect pathway (01 receptors) and excitatory on the direct pathway (0 1 receptors). Thus, the action of dopamine is, overall, excitatory. Lesions of the basal ganglia include the following: Lesions of the globus pallidus result in inability to maintain postural support. Lesions of the subthalamic nucleus are caused by the release of inhibition on the contralateral side. result in wild, flinging movements (e.g., hemiballismus). Lesions of the striatum are caused by the release of inhibition. result in quick, continuous, and uncontrollable movements. occur in patients with Huntington disease. Lesions of the substantia nigra are caused by destruction of dopaminergic neurons. occur in patients with Parkinson disease. Since dopamine inhibits the indirect (inhibitory) pathway and excites the direct (excitatory) pathway, destruction of dopaminergic neurons is, overall, inhibitory. Symptoms include lead-pipe rigidity, tremor, and reduced voluntary movement. H. Motor cortex 1. Premotor cortex and supplementary motor cortex (area 6) are responsible for generating a plan for movement, which is transferred to the primary motor cortex for execution. The supplementary motor cortex programs complex motor sequences and is active during ·mental rehearsal· for a movement. 56 BRS Physiology 2. Primary motor cortex (area 4) is responsible for the execution of movement. Programmed patterns of motoneurons are activated in the motor cortex. Excitation of upper motoneurons in the motor cortex is transferred to the brain stem and spinal cord, where the lower motoneurons are activated and cause voluntary movement. is somatotopically organized (motor homunculus). Epileptic events in the primary motor cortex cause jacksonian seizures, which illustrate the somatotopic organization. V. HIGHER FUNCTIONS OF THE CEREBRAL CORTEX A. Electroencephalographic (EEG) findings EEG waves consist of alternating excitatory and inhibitory synaptic potentials in the pyramidal cells of the cerebral cortex. A cortical evoked potential is an EEG change. It reflects synaptic potentials evoked in large numbers of neurons. In awake adults with eyes open, beta waves predominate. In awake adults with eyes closed, alpha waves predominate. During sleep, slow waves predominate, muscles relax, and heart rate and blood pressure decrease. B. Sleep 1. Sleep-wake cycles occur in a circadian rhythm, with a period of about 24 hours. The circadian periodicity is thought to be driven by the suprachiasmatic nucleus of the hypothalamus, which receives input from the retina. 2. Rapid eye movement (REM) sleep occurs every 90 minutes. During REM sleep, the EEG resembles that of a person who is awake or in stage I nonREMsleep. Most dreams occur during REM sleep. REM sleep is characterized by eye movements, loss of muscle tone, pupillary constriction, and penile erection. Use of benzodiazepines and increasing age decrease the duration of REM sleep. C. Language Information is transferred between the two hemispheres of the cerebral cortex through the corpus callosum. The right hemisphere is dominant in facial expression, intonation, body language, and spatial tasks. The left hemisphere is usually dominant with respect to language, even in left-handed people. Lesions of the left hemisphere cause aphasia. 1. Damage to Wernicke area causes sensory aphasia, in which there is difficulty understanding written or spoken language. 2. Damage to Broca area causes motor aphasia, in which speech and writing are affected, but understanding is intact. D. Learning and memory Short-term memory involves synaptic changes. Long-term memory involves structural changes in the nervous system and is more stable. Bilateral lesions of the hippocampus block the ability to form new long-term memories. l!1lD'!ltlfj Neurophysiology t a b I e CSF~ 2.9 57 Comparison of Cerebrospinal Fluid (CSF) and Blood Concentrations Blood CSF Blood Na+ K+ Mg2+ Cl- Ca 2+ Creatinine HC0 3- Glucose Osmolarity Cholesterol* Protein* "Negligible concentration in CSF. VI. BLOOD-BRAIN BARRIER AND CEREBROSPINAL FLUID (CSF) A. Anatomy of the blood-brain barrier It is the barrier between cerebral capillary blood and the CSE CSF fills the ventricles and the subarachnoid space. It consists of the endothelial cells of the cerebral capillaries and the choroid plexus epithelium. B. Formation of CSF by the choroid plexus epithelium Lipid-soluble substances (C0 2 and 0 2) and H 2 0 freely cross the blood-brain barrier and equilibrate between blood and CSE. Other substances are transported by carriers in the choroid plexus epithelium. They may be secreted from blood into the CSF or absorbed from the CSF into blood. Protein and cholesterol are excluded from the CSF because of their large molecular size. The composition of CSF is approximately the same as that of the interstitial fluid of the brain but differs significantly from blood (Table 2.9). CSF can be sampled with a lumbar puncture. C. Functions of the blood-brain barrier 1. It maintains a constant environment for neurons in the CNS and protects the brain from endogenous or exogenous toxins. 2. It prevents the escape of neurotransmitters from their functional sites in the CNS into the general circulation. 3. Drugs penetrate the blood-brain barrier to varying degrees. For example, nonionized (lipid-soluble) drugs cross more readily than ionized (water-soluble) drugs. Inflammation, irradiation, and tumors may destroy the blood-brain barrier and permit entry into the brain of substances that are usually excluded (e.g., antibiotics, radiolabeled markers). VII. TEMPERATURE REGULATION A. Sources of heat gain and heat loss from the body 1. Heat-generating mechanisms-response to cold a. Thyroid hormone increases metabolic rate and heat production by stimulating Na+, K+-adenosine triphosphatase (ATPase). b. Cold temperatures activate the sympathetic nervous system and, via activation of~ receptors in brown fat, increase metabolic rate and heat production. c. Shivering is the most potent mechanism for increasing heat production. Cold temperatures activate the shivering response, which is orchestrated by the posterior hypothalamus. 58 BRS Physiology a-Motoneurons and y-motoneurons are activated, causing contraction of skeletal muscle and heat production. 2. Heat-loss mechanisms--response to heat a. Heat loss by radiation and convection increases when the ambient temperature increases. The response is orchestrated by the anterior hypothalamus. Increases in temperature cause a decrease in sympathetic tone to cutaneous blood vessels, increasing blood flow through the arterioles and increasing arteriovenous shunting of blood to the venous plexus near the surface of the skin. Shunting of warm blood to the surface of the skin increases heat loss by radiation and convection. b. Heat loss by evaporation depends on the activity of sweat glands, which are under sympathetic muscarinic control. B. Hypothalamic set point for body temperature 1. Temperature sensors on the skin and in the hypothalamus "read" the core temperature and relay this information to the anterior hypothalamus. 2. The anterior hypothalamus compares the detected core temperature to the set-point temperature. a. H the core temperature is below the set point, heat-generating mechanisms (e.g., increased metabolism, shivering, vasoconstriction of cutaneous blood vessels) are activated by the posterior hypothalamus. b. H the core temperature is above the set point, mechanisms for heat loss (e.g., vasodilation of the cutaneous blood vessels, increased sympathetic outflow to the sweat glands) are activated by the anterior hypothalamus. 3. Pyrogens increase the set-point temperature. Core temperature will be recognized as lower than the new set-point temperature by the anterior hypothalamus. As a result, heatgenerating mechanisms (e.g., shivering) will be initiated. C. Fever 1. Pyrogens increase the production of interleukin-1 (IL-l) in phagocytic cells. Macrophages release cytokines into the circulation, which cross the blood-brain barrier. IL-l acts on the anterior hypothalamus to increase the production of prostaglandin E2 Prostaglandins increase the sat-point temperature, setting in motion the heat-generating mechanisms that increase body temperature and produce fever. 2. Aspirin reduces fever by inhibiting cyclooxygenase, thereby inhibiting the production of prostaglandins. Therefore, aspirin decreases the sat-point temperature. In response, mechanisms that cause heat loss (e.g., sweating, vasodilation) are activated. 3. Steroids reduce fever by blocking the release of arachidonic acid from brain phospholipids, thereby preventing the production of prostaglandins. D. Heat exhaustion and heat stroke 1. Heat exhaustion is caused by excessive sweating. As a result, blood volume and arterial blood pressure decrease and syncope (fainting) occurs. 2. Heat stroke occurs when body temperature increases to the point of tissue damage. The normal response to increased ambient temperature (sweating) is impaired, and core temperature increases further. E. Hypothermia results when the ambient temperature is so low that heat-generating mechanisms (e.g., shivering, metabolism) cannot adequately maintain core temperature near the set point. F. Malignant hyperthermia is caused in susceptible individuals by inhalation anesthetics. is characterized by a massive increase in oxygen consumption and heat production by skeletal muscle, which causes a rapid rise in body temperature.
