E3. Neurology Flashcards
What are the 9 steps/approaches to a patient with neurological dysfunction?
- Determine case signalment and owners complaint.
- Obtain history.
- Perform a general physical examination.
- Perform a neurological examination and localize lesion/s.
- Compile differential diagnosis list.
- Collect minimum database.
- Do special diagnostic tests.
- Establish prognosis with and without treatment.
- Initiate therapy if necessary.
True or false for case signalment:
Most neurological diseases affect animals of certain age, breed or sex.
True.
What might determination of the onset and progression of neurological signs indicate?
Possible etiologies
What might a peracute onset of neurological signs suggest? (Possible etiology)
Trauma or disc extrusion.
What might a slow progressive development of neurological signs be more likely to suggest? (Possible etiologies)
Degenerative, neoplastic or metabolic changes.
On your general physical examination if you see dysfunction in the nervous system and other organ systems what might this suggest? Give examples.
Polysystemic disorders might be present.
Examples are distemper, metabolic problems (hepatic encephalopathy, renal failure), neoplasia.
What can influence the prognosis and treatment of neurological problems? (These could be found on a general physical examination) (general think of summation)
Concurrent diseases
What is the purpose of a neurological examination?
Localized neurological lesions in animals with neurological dysfunction.
Where are your upper motor neurons (UMN) cell bodies and axons located? (4)
Situated in the cerebral cortex and brainstem (cell bodies) and in the brain stem or spinal cord (axons)
Where are your lower motor neurons (LMN) cell bodies and axons located?
Cell bodies: brainstem (cranial nerves) or ventral horn of the spinal cord (peripheral nerves).
Axons: runs in the cranial or peripheral nerves and supply muscles and glands of the body.
What is able to control the lower motor neurons?
Voluntary control (via UMNs) and can also be controlled by reflex activity in the spinal cord.
Look at the bottom of page 2 in top of page 3
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What type of affected does upper motor neurons have on the lower motor neurons spinal reflexes tested in the neurological examination?
It will inhibit.
What happens if you lose your upper motor neurons?
Loss of UMNs therefore results in intact or hyperactive spinal reflexes. It also results in paralysis/ pareseis, mild muscle atrophy due to disuse, normal/increased tone in limb muscles, and abnormal reflexes such as the crossed- extensor reflex (see below).
What happens if you lose your lower motor neurons?
(1) paresis or paralysis,
(2) hyporeflexia or areflexia,
(3) early and severe muscle atrophy which may result in fibrosis and contracture of affected muscles after several weeks,
(4) loss of muscle tone.
What type of neurons is responsible for carrying conscious proprioception and pain and touch information to the contralateral cerebral cortex?
Long tract sensory neurons
What happens if there is a lesion in the long tract sensory nerves? (5)
(1) anesthesia or hypoesthesia caudally to the lesion,
(2) normoreflexia,
(3) abnormal positioning of the feet (lack of conscious proprioception),
(4) dysmetria (usually hypermetria - steps are longer and higher than normal, and
(5) ataxia (incoordination - a swaying staggering gait with occasional hypermetria and catching of limbs dd. weakness - stiff stilted gait with short strides, postural tremor, usually collapses or rests after a few strides)
look at page 3
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Lesions between the 6th cervical spinal cord segment (lying within the vertebral canal of vertebra C6) and the 2nd thoracic spinal cord segment (in T2) affect what?
Affect the cell bodies of the LMN to the forelimb – radial nerve etc.
Lesions in the C6 to T2 spinal cord segments can cause what?
Cause LMN and segmental sensory signs to one front limb (if the lesion is unilateral) or both front limbs (if the lesion is bilateral). In the hind limbs, signs will also be seen but these will be UMN and long tract sensory.
What can a lesion in the spinal cord segment of T3 to L3 cause?
Lesions in spinal cord segments T3 to L3 cause UMN and long tract sensory signs in the hind limbs. Lesions caudal to L3 will involve the cell bodies of the nerves of the hind limbs (femoral, sciatic, etc) and this will therefore give rise to LMN and segmental sensory signs in the hind limbs.
Look at page 4
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What can cause hyperreflexia?
Loss of upper motor nor on inhibition to extensor spinal neurons. It can also be due to the narration hypersensitivity where partially innervated spinal motor neurons become more sensitive to afferent stimulation.
What can cause cross extensor reflex?
There are long spinal reflexes between limbs that are usually suppressed by UMNs. Damage to the UMNs releases this inhibition and flexion of one limb in response to a noxious stimulus is accompanied by extension of the contralateral limb.
What can cause Schiff-Sherrington phenomenon?
Following damage (usually severe) to the spinal cord (T3 to L3) the forelimbs may become rigidly extended with marked increase in extensor tone. Voluntary movement is still present although markedly reduced by the hypertonia. Ascending spinal cord tracts in the spinal cord from L1 to L5 inhibit extensor muscles of the thoracic limbs. Transection of these pathways removes the inhibition and results in extension of the thoracic limbs.
What are the six things that must be done in sequence and neurological examination?
- Observation of mental status, posture and gait.
- Palpation of muscular and skeletal systems.
- Evaluation of postural reactions.
- Evaluation of cranial nerves.
- Evaluation of spinal nerves.
- Evaluation of sensation.