Ireland Neurophysiology: Test 3
Terms in this set (71)
An imaginary line drawn through the spinal cord up to the front of the brain.
How are anatomical directions understood?
Relative to the neuraxis.
Toward the head
Toward the tail
Toward the "belly"
Toward the back (top of the head)
Locations in the brain
1. Ipsilateral: same side of the brain
2. Contralateral: opposite side of the brain
The brain can be sectioned into three planes, and each section provides a different view of the internal anatomy of the brain.
1. Sagittal (cut down the hemispheres)
2. Coronal (vertical cut)
3. Horizontal (horizontal cut)
Methods of Brain Study
1. Examine the effects of brain damage.
2. Examine the effects of stimulating some part of the brain.
3. During some kind of behavior, record what happens in the brain.
4. Correlate brain anatomy with behavior.
1. Golgi stain method: highlight individual neurons.
2. Myelin stains: emphasize white matter... neural pathways.
3. Nissl stains: emphasize cell bodies of neurons.
The removal or destruction of the portion of the brain of a laboratory animal; presumably, the functions that can no longer be performed are the ones the regions previously controlled.
Legion studies (wound or injury)
1. Radio frequency lesioning: heat applied through an electrode destroys tissue
2. Excitotoxic lesioning: intracerebral injection of excitatory amino acid (i.e. Kainic Acid) stimulates neurons to exhaustion (death).
Brain surgery using a stereototaxic apparatus to position the electrode or cannula in a specific region (position of the brain).
Bregma: the junction of the sagittal and coronal sutures of the skull that serves as a reference point for surgery.
Temporary inactivation of a specific brain region by the infusion of a local anesthetic (allows animal to serve as it's own control).
Device surgically implanted between the skull and brain, chilled liquid is circulated through stainless steel tubes, produces temporary lesion while animal is awake/alert.
Labeling of axons and terminal buttons of neurons whose cell bodies are located in a particular region (i.e. PHA-L) Note: Tracing efferent connections
Labeling of cell bodies that give rise to terminal buttons that form synapses with cells in a particular region (i.e. fluorogold) taken up by terminal buttons and carried back to cell bodies.
Note: Tracing afferent connections
Computerized Tomography (CT)
Uses an x-ray beam to scan the brain from all angles. Provide a gross picture of the brain.
Magnetic Resonance Imaging (MRI)
Show a lot more detail than a CT scan.
Uses radioactive molecules to highlight the most active parts of the brain.
Functional MRI (fMRI)
Basically the same as a PET scan.
A single cell
Clusters of cell body
PNS: Ganglia (ganglion-- singular)
CNS: Nuclei (nucleus-- singular)
Clusters of axons
PNS: Nerves (i.e. optic nerve)
CNS: Tracts (i.e. optic tract)
Where neuron cell bodies are concentrated (few myelinated).
Bundles of axons, mostly myelinated.
Neuron classification by function
Afferent: coming into CNS
Efferent: away from CNS
A groove that separates a gyrus.
A protuberance on brain surface.
A long deep sulcus.
Peripheral Nervous System (PNS) Functions
1. Transmit information to muscles (motor pathways)
2. Arise from sensory surfaces (sensory pathways)
3. Transmit info in both directions between CNS and internal organs
Note: 1&2 somatic; 3 autonomic
The autonomic nervous system is divided into...
1. Sympathetic Nervous System (arouses)
2. Parasympathetic Nervous System (does not arouse)
1. Heart and blood pressure increases
2. Respiration accelerates, blood sugar is released from the liver.
3. Adrenaline, noradrenaline released from the adrenal glands
4. Fight or flight
1. Heartbeat slows
2. Blood pressure reduces
3. Respiration levels
4. Your body experiences visceral response typical of periods of rest snd relaxation
5. Rest and digest
Spinal cord functions
1. Spinal reflexes (simple stereotyped motor for basic movement... inborn, unlearned)
2. Convey information to and from the brain
Spinal cord info
1. It is a segmented structure, and each segment has in each side a sensory nerve and a motor nerve. Each segment sends sensory info to the brain and receives motor commands from the brain.
2. The spinal cord is comprised of gray and white matter
a. Gray matter: located in the center of the spinal cord and is densely packed with cell bodies and dendrites.
b. White matter: comprised mostly of myelinated axons that carry info from the gray matter to the brain or other areas of the spinal cord.
Label cross section of the spinal cord
1. Gray matter
2. Spinal nerve
3. Central canal
4. Ventral root
5. Dorsal root
6. Dorsal root ganglion
7. Spinal nerve
1. Forms the outer structure of the cerebral hemispheres. The cortex (bark or shell) surface is convoluted grooves.
2. Corpus callosum connects the two hemispheres together.
Label lobes of the cerebral cortex and name their functions
1. Frontal lobe (receives and coordinates messages from other lobes, motor control, speech production)
2. Temporal lobe (hearing, language, comprehension, memory, and some emotional control)
3. Central fissure (separates frontal and parietal lobes)
4. Occipital lobe (vision and visual perception)
5. Lateral fissure (separates frontal and temporal lobe)
6. Parietal lobe (receives info about pressure, pain, touch, and temperature)
Primary v. Association cortex
Association cortex is the cerebral cortex outside the primary areas. It is essential for mental functions that are more complex than detecting basic dimensions or sensory stimulation, for which primary sensory areas appear to be necessary.
Label these parts on the brain (Primary v. Association cortex)
LOOK UP A PICTURE
1. Primary auditory cortex
2. Auditory association cortex
3. Visual association cortex
4. Primary visual cortex
5. Primary motor cortex
6. Primary somatosensory cortex
7. Somatosensory association cortex
Label the Hindbrain with functions
1. Medulla (medulla oblongota): breathing, heart rate, vomiting, coughing, blood vessels
2. Pons: regions involved in motor control and sensory analysis (sleep/arousal)
3. Reticular formation: sleep and arousal, temperature regulation, motor control. Runs from midbrain into medulla and pons.
4. Cerebellum: motor coordination and involvement in language acquisition and cognition.
Midbrain (do not need to label)
Two bumps are visible on the dorsal surface of the midbrain
1. Superior colliculi: receives visual information
2. Inferior colliculi: receives information about sound
Forebrain (covered by cerebral cortex). Label with functions.
1. Thalamus: complex swirl of nuclei that act as go-betweens for the cerebral cortex. Almost all sensor info enters thalamus.
2. Hypothalamus: under the thalamus packed with distinct nuclei with vital functions-- hunger, thirst, and temperature regulation.
3. Pituitary gland: controls almost all hormone secretion.
4. Basal ganglia: occupy large space within cerebral hemispheres (NO LABEL).
4. Limbic system: hippocampus (role in memory). Amygdala (role in emotion). (NO LABEL).
Label the ventricles
1. Lateral ventricles.
2. Cerebral aqueduct.
3. Third ventricle.
4. Fourth ventricle.
Functions of the cerebrospinal fluid (CSF)
1. Acts as a shock absorber for the brain... the brain floats in CSF as the brain moves... thus head movements do not result in forceful shifting of the brain cavity.
2. It mediates between blood vessels and brain tissue in the exchange of materials, including nutrients and hormones.
3. It provides buoyancy to help support the weight of the brain.
The brain and spinal cord are protected by a series of membranes termed meninges.
1. Dura mater: outer (thick layer for protection)
2. Arachnoid: middle layer. Overlies the arachnoid space (CSF). Blood vessels run through the arachnoid layer.
3. Pia mater: inner layer. Overlies every detail of outer brain (thin).
The brain has no pain receptors, but the meninges do. Swollen blood vessels in the meninges are the cause of migraine headaches.
Receives 20% of blood flow from heart. Blood flow is continuous unlike other parts of the body that receive it according to need.
Blood flow is necessary since... 1. Brain cannot store glucose (fuel) and 2. Unlike muscles, it cannot deal with temporary lack of oxygen.
Neoplastic Responses to Nervous system damage
Recovery... (Real v. compensatory)
Recovery of function after brain damage is poorly understood...
1. Difficult to conduct controlled experiments with brain damage patients.
2. Compensatory changes may confuse real recovery. ex: cerebral edema (brain swelling). Improvement may not be due to real recovery but cognitive reserve which allowed them to accomplish tasks in alternative ways. Education + intelligence = cognitive reserve. Gradual improvement may reflect the learning of new cognitive and behavioral strategies.
Diagnosis of Brain Damage
Both are common neuropsychological batteries used to assess cognitive deficits resulting from brain damage.
They are not used as much anymore.
1. Meningiomas: Tumors that are encapsulated by their own membrane. They affect the brain by compression as they grow and force the brain up against the skull. They can be removed surgically with little future risk and are benign. 20%.
2. Infiltrating tumors: They diffuse through the brain tissue in fingerlike projections... Thus malignant... Almost impossible to remove it all surgically. 70%.
3. Metastatic: Originate in another part of the body but travel to the brain via the bloodstream. Prognosis not as good since tumors are not confined by metastasizing. 10%.
Formation of Thrombi and Emboli
Thrombus: some material that starts gathering and builds up until it blocks an artery.
Embolus: breaks off of thrombus and occludes smaller artery.
Note: No longer epilepsy due to negative connotation.
Second only to stroke as the most impactful neurological disorder.
If neurons involved in the motor system are involved, a convulsion is experienced.
Classification of seizure disorders
1. Partial: focus or irritation are specific and restricted to small areas of the brain.
Generalized: Widespread and involving most of the brain.
2. Simple: no loss of consciousness
Complex: loss of consciousness.
Grand mal seizure: Generalized tonic-clonic.
Tonic: beginning of grand mal. Rigid muscles. At this point, the person is unconscious. Phase lasts about 15 seconds.
Clonic: Muscles being trembling. Then jerky. Fast to slow. After 30 seconds relax.
Note: Absence seizures (petit mal). Lasts a few seconds. Stare off, often blinking repeatedly. Usually don't notice. Can occur several hundred times a day.
Chronic Traumatic Encephalopathy (CTE)
1. Under the category of Traumatic Brain Injury (TBI).
2. A progressive degenerative disease, diagnosed post-mortem (or brain biopsy while alive) in individuals with a history of multiple concussions and other forms of head injury. (After one concussion, it is much easier to have another one).
3. A variant... Dementia Puglistica (DP)... Boxing.
4. Brain pathology: reduction in brain weight. Enlargement of lateral (53%)/third ventricles (29%) (filling space where the brain should be).
5. Atrophy of Lobes: Frontal (36%), Temporal (31%), Parietal (22%), and Occipital (3%).
6. Atrophy of thalamus, brainstem, cerebellum... later progression indicates marked atrophy in hippocampus and amygdala.
7. Tau Deposition: accumulation of tau protein linked to tangles in microtubules in axons... found in dementia, alzheimers, etc., and associated with poor brain recovery after trauma.
8. Physical/mental symptoms... disorientation, confusion, vertigo, headaches, poor judgement, dementia, slowed muscular movement, staggered gait, impeded speech, and tremors.
Traumatic Brain Injury (TBI)
1. Closed v. open head injury
2. Neurobehavioral effects: Most common complaints are concentration and memory. Handicapped more by personality/emotional disturbances than cognitive/physical disturbances.
Neoplastic disease (brain tumor)
1. Speed of growth, size, location important.
2. Right vs. left hemisphere damage.
Chronic alcohol abuse
1. Neuronal changes that include loss of dendrites (hippocampus-- memory).
2. Enlargement of ventricles.
3. Widening of sulci.
4. Severe abuse: Wernicke-Korsakoff's syndrome: Anterograde amnesia (only remember current conversation). Confabulation (falsification of memory).
1. Neuritic plaques and neurofibrillary tangles and extra amyloid proteins.
2. Neuronal loss.
3. Shrinkage, brain atrophy.
4. Depletion of NTs.
5. Anterograde/retrograde amnesia.
6. Personality changes... agitation, delusions.
Vascular dementia (stroke)
(connect with contusions) Blockage of an artery leading to death of neural tissue due to: 1. Insufficient blood supply (infraction). 2. Bleeding in/around the brain (hemorrhage).
Symptoms include motor weakness, loss of feeling on opposite side of body, and non-fluent aphasia.
Dementia syndrome of depression (pseudomentia)
1. Some depressed elderly indicate cognitive deficits that mime dementia.
2. Memory loss, loss of cognitive skills.
Contusions v. concussions
1. Contusions: damage to the cerebral vascular system which leads to hemorrhaging and a pooling of blood in the brain (hematoma).
2. Concussions: primarily a jarring or a shock to the brain leading to a temporary effect on consciousness. Repeated concussions may lead to punch-drunk syndrome or CTE (chronic traumatic encephalopathy).
Coup (primary impact)
Contrecoup (secondary impact)
Not good to keep people awake after a concussion... In fact they need to sleep. They used to think you should keep them awake for 6 hours and this would prevent a coma. If someone cannot stay awake though, w/in six hours, take them to the ER.
when you cut the axon
when it goes away from the cell.
Works backward and will destroy entire cell.
Any progressive change in the way the nervous system responds to a stimulus as a result of experience.
Brain Recovery: early v. late damage
1. Early damage: uncontrollable seizures during the first year of life may lead to the removal of the damaged hemisphere (successful deals with seizures 70% of the time).
A. Left hemisphere removal: child is able to speak, write, and use language. Somehow, the right hemisphere develops these functions. However, the right hemisphere cannot assume its own functions. Something must be sacrificed (i.e. special organization). Also, some functions are completely lost, even if removal occurs very early and the L.H. is removed, the right side of the body would be paralyzed. However, early brain damage does show that the remaining hemisphere has flexibility or plasticity to develop.
B. Case study: at 5 and 1/2, left hemisphere removed (seizures). Tested at 27 to see which functions R.H. had assumed. Paralyzed on right side of body. No sensations on right side, and blind in right visual area (the R.H. does not assume sensory and motor functions found in the L.H.). Completed college.
2. Late damage: Either hemisphere can develop language functions until the ages of 5-7. After age 10, the brain damage then results in serious speech and language problems if the L.H. is damaged. At this point, the R.H. lacks the flexibility to assume these functions. Damage to the L.H. before 10 may result in:
A. Aphasia (complete): no speech.
B. Broca's Aphasia: slow and labored speech.
But the prospects of recovery are very good. After 10, the prospects for recovery are very poor.
3. Reorganization of sensory representations.
Considerable redundancy exists throughout the CNS so that even though there may be apparent recovery from brain damage, it is only because impaired behavior is mediated by alternative redundant, uninjured circuits. This may occur since during development, many axons for tentative connections with a given postsynaptic neuron (competitive process leads to activation of some, but not all). Upon injury, these previously ineffective axons may be activated as with compensatory mechanisms.
Mechanisms of recovery from brain damage: not neural recovery
1. Diachisis: refers to the decreased activity of neurons after they have lost part of their input when other neurons were damaged. I.e. the cells responsiveness is temporarily disrupted.
Might result from BBB change as blood-borne substances, normally prevented from entering the brain, enter to produce toxicity. This leads to temporary nonfunctioning of surrounding cells and behavior deficits. As time passes, BBB is reestablished and toxic materials are removed by glial cells (functioning seems to improve).
2. Denervation supersensitivity: heightened sensitivity to the NT after the destruction of incoming axon. Results in increased numbers of receptors on the surface of the cell or from changes within the cell. Explanation for massive loss of DA containing axons in the Substantia Nigra of Parkinson's patients before they begin to show symptoms:
A. After the loss of axons, remaining axons compensate by increasing their release of DA.
B. Further loss leads to receptors on postsynaptic membrane developing denervation supersensitivity.
C. A and B compensate for a loss of up to 70-90% of axons.
REAL Neural Recovery (CNS/PNS?)
1. Axonal sprouting: if one set of axons is destroyed, then the synaptic spaces become vacant. Within a few days to a few weeks, the uninjured axons that remain in the surrounding area form new branches (collateral sprouts) that attach to the vacant synapses.
Enhance or retard (misconnecting TV wires). Spasticity noted.
A. Growing view is that injury to the NS might release nerve growth factors. Researchers have reported that chemicals in the area surrounding brain injury contain a growth promoting substance.
2. Neural regeneration: regrowth of damaged neurons is virtually nonexistent in the CNS. In the PNS, regrowth from the proximal stump of a damaged nerve begins 2-3 days after damage-- what happens next depends on the nature of the injury.
3. Axotomy: severing an axon or bundle of axons. Results in 2 kinds of neural degeneration:
1. Anterograde: degeneration of distal segment. Becomes badly swollen within a few days. Breaks into fragments (usual course).
2. Retrograde: degeneration of proximal segment; changes in cell body occur in 2-3 days. Either:
1. Degenerative: decreases in size of cell body usually means cell body will eventually die.
2. Regenerative: increase in size of cell body usually means cell body is involved in massive protein synthesis designed to replace degenerated axon. However, no guarantee: if axon doesn't synaptically connect with target, neuron will probably have a chance to live.
Recovery by neurotransplantation
1. Transplanting fetal tissue: early positive signs (late 1980s).
A. Monkey model of Parkinson's disease. Fetal substantia Nigra transplants were accepted releasing DA and reducing tremor.
B. Parkinson's patients (early 1990s): fetal substantia nigra implants. Early signs promising as implants survive and release DA... Some improvement. Unfortunately, 15% displayed uncontrollable writhing and chewing movements about one year after the surgery.
Thus, fetal neurotransplatation has come under debate. Alternative: adrenal medulla autotransplanation (from own adrenal medulla cells). Release smaller amounts of DA.
2. Transplanting stem cells (2000-present)
Stem cells are multipotent i.e., have the capacity to develop into many types of mature cells.
Break-through study in 2000 (McDonald et. al.) injected embryonic sucural stem cells into an area of spinal damage in rats rendered paraplegic by a blow. The stem cells migrated to areas around the damaged site where they developed into mature neurons. The rats became capable of supporting their weight and could walk... albeit awkwardly.
Triggered a frenzy of research activity.
Fetal to adult stem cells.
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