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5 Cards in this Set
- Front
- Back
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Describe the visual pathway
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❤NEURON 1:
-is the bipolar cell of the retina, which receives impulses from the neuroepithelial cells of the retina (rods & cones) ❤NEURON 2 -is the ganglion cell of the retina -the optic nerves converge in the midline just above the pituitary gland to form the optic chiasm and then diverge again. -at the chiasm, there is a partial crossing or decussation of optic nerve fibers; 60% of the fibers from each nerve cross to the opposite side, whereas the other 40% remain uncrossed. -the optic tracts contain remixed (partially crossed) optic nerve fibers that extend from the chiasm -Most axons of the ganglion cells in the optic tracts project to the lateral geniculate nucleus in the thalamus -the remaining 20% bypass the lateral geniculate nucleus or send terminal filaments to the rostral colliculus or pretectal area, to control pupil size and to coordinate movements of the eyeball, as well as the head and neck ❤NEURON 3 -has its cell body in the LGN and projects axons along the optic radiation to the visual cortex which lives in the occipital lobe of the brain -vision doesn't begin to occur until impulses from the optic nerve reach this part of the brain and are decoded to provide meaningful information about the outside world |
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Describe the menace response
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-is a learned response that appears at 14-16 weeks in puppies and kittens that produces a blink in response to rapidly moving objects that approach the eye
-neurons in the occipital cortex project via projection fibers to the motor cortex, where they synapse with other neurons who send their axons via the internal capsule and crus cerebri to synapse on the nuclei in the pons -nuclei in the pons then send their axons into the contralateral cerebellar hemisphere (for coordination) to synapse on further neurons which then send axons down into the pons (back to the side of the origin of the signal) where they ultimately synapse in the facial nerve nucleus - to drive the blink that occurs -testing vision during the clinical exam involves menacing the eye with a fast moving object (usually a hand) and looking for a blink -ABSENT: if absent but the pupillary response is still intact, this implies the animal cannot see out of the affected eye, BUT the lesion is not in the optic nerve or eye, but rather in the brain (known as cortical blindness or amaurosis, common in animals with prosencephalic lesions) |
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What are the other pathways involving the optic nerve?
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-the 20% of endings of axons in the optic nerve that do not reach the lateral geniculate nucleus synapse in the ROSTRAL COLLICULUS in the midbrain to serve 4 other functions
1) CONTROL OF EYEBALL MOVEMENTS -from the rostral colliculus, neurons project to the motor nuclei of CN III, IV, and VI of both sides (ie. bilaterally) to coordinate movements of the eyeball in response to visual stimuli, in particularly for reflex movements of the eyes towards the flash of light -this pathway is also important for coordinating an object under observation focused on the area centralis of the retina -note that this pathway is different from that that enables voluntary movements of the eyeballs 2) PUPIL CONSTICTION -neurons in the rostral colliculus project to both the left and right parasympathetic nuclei of the oculomotor nerve (known as the Edinger-Westphal nuclei in humans) -these enable both pupils to constict in response to light shone in either eye (although the response is strongest in the eye recieving visual input) 3) CONTROL OF TURNING OF THE HEAD & NECK -from the rostral colliculus neurons send axons which decussate and descend through the brain and into the spinal cord forming the tectospinal tract -this allows for reflex turning of the head and neck towards a sudden source of light or movement 4) PROJECTIONS INTO THE RETICULAR ACTIVATING FORMATION -some neurons from the rostral colliculi project into the reticular activating formation (also known as the ascending reticular formation) to provide general arousal stimuli to the cerebral cortex |
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What are the clinical signs of forebrain disease?
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-the main (most specific) sign of forebrain disease is seizures
-however, other signs occur that reflect the normal functions performed by the forebrain ●blindness (with intact papillary light reflex) ●proprioceptive deficits ●circling ●compulsive walking ●head-pressing ●changes in behavior ●changes in sensitivity to touch stimuli ●hemineglec/hemiinattention syndrome -almost all of these signs occur on the side of the body contralateral to the site of the lesion, with the exception of circling which occurs towards the side of the lesion |
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What is a seizure? What kinds of seizures are there? What is the aetiology of seizures?
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❤SEIZURE - is a transient and involuntary change in behavior or neurological status due to the abnormal activity of populations of central nervous system neurons
-the neuronal activity is usually excessive and synchronous in character -a seizure may be described as a paroxysmal cerebral dysrhythmia that has a sudden onset, ceases spontaneously and has a tendency to reoccur ❤EPILEPSY = seizures that are recurrent and of unknown cause ❤TYPES ●SYMPTOMATIC - secondary due to a structural brain lesion, reactive (due to extracranial metabolic or toxic insult) ●IDIOPATHIC - no underlying eitology Can be classified by clinical appearance: ●PARTIAL OR FOCAL SEIZURES - begin in a discrete cerebrocortical region and may or may not generalize -due to a structural lesion ●GENERALIZED SEIZURES - due to generalized brain disturbance - symmetrical, associated with a loss of consciousness and may or may not involve motor activity -may be preceded by an aura (restless, anxious, hyper excitability) ❤PHASES: -the ictal period is the actual seizure event and the post ictal phase is the period immediately after a seizure -the length of the post ictal phase can vary (minutes to days) and may not be related tot he severity of the seizure -post ictal signs can include exhaustion, disorientation, hunger, circling, ataxia, blindness, and proprioceptive deficits -persistent asymmetrical signs will indicate a structural lesion ❤ETIOLOGY -uncertain, but a burst firing quality of regionally specific neuronal sub-populations is likely to be involved -these cells may express a marked prolonged depolarization phase (paroxysmal depolarization shift) -seizures can be precipitated by decreasing the activity of the reticular activating system (eg. sleep) Injuries to the brain appear to change the inherent excitability of glutamatergic neurons. The glutamate receptor type, number, spatial distribution and sensitivity may change after injury. A dynamic enhancement of synaptic strength due to activity in excitatory circuits may also be involved (increased EPSP). Brain injury (ischaemia, hypoxia and trauma) may also cause loss of inhibitory neurons (gammaaminobutyric acid- GABA) and synapses. Excessive neuronal activity can cause the accumulation of potassium and glutamate if the astrocytes are dysfunctional. The accumulation of potassium extracellularly can cause depolarisation of neighbouring axon terminals and blunt potassium efflux to prolong the paroxysmal depolarisation shift. Glutamate can accumulate at excitatory synapses and activate post synaptic receptors. The ease with which seizure activity may spread to involve other brain areas may change with time. SUMMARY -glutamate receptor type, number or spatial distribution may change -brain injury may cause hypoxia which may cause loss of inhibitory neurons -this leads to excessive neuronal activity and accumulations of K+ and glutamate if astrocytes are dysfunctional -the K+ will cause depolarization of neighboring axon terminals -glutamate can activate the post synaptic receptors |
