Neurolocalisation, CN Neuropathies Flashcards
opisthotonus with extensor rigidity of forelimbs, but hips are flexed in the HLs
DecereBELLate rigidity
rigid extension of neck and all 4 limbs
Decerebrate rigidity = midbrain (or rostral cerebellum)
Opisthotonus = spasm of muscles of neck causing backward arching of the head neck and spine
Dog with Altered mentation circles to left (wide); sensory deficits on right side of face and placement deficits in right side paws with normal reflexes and tone in all limbs
Left Forebrain lesion
Contralateral placement deficits
Contralateral facial sensory deficits
Ipsilateral circles/head turn (pleurothotonus)
Gait and muscle tone usually not affected
Difference between paresis and plegia
PAresis is weakness/inability to support weight
Plegia = loss of function of motor unit
Features of cerebellar ataxia
Dysmetria
Hypermetria (prolonged flexion)
Intentional tremors
Wide base posture at rest with no proprioceptive deficits
cause and features of proprioceptive ataxia
spinal cord lesions, which cause disruption of the ascending GP tracts that relay spatial location and degree of muscle contraction of the head neck and limbs
–> incoordination
–> truncal sway,
–> abnormal limb stance and gait with limbs crossing over each other as the animal walks.
Frequently have concurrent paresis because descending (UMN) pathway and ascending GPO pathways are located near each other in spinal cord
Features of vestibular ataxia
Loss of orientation of the head with respect to eyes, neck, limbs and trunk. Affected animals may lose their balance, drift, lean or fall or in one direction. Usually towards the lesion
Head tilt TOWARDS lesion (unless paradoxical cerebellar in which case trust the postural deficits)
If peripheral lesion then normal strength and proprioception
In central disease proprioceptive and postural reaction deficits (ALWAYS ipsilateral to head tilt)
What controls postural reactions
To maintain normal upright position an increased load on a supporting limb/s requires increased extensor tone - this is accomplished through spinal reflexes, but for smooth coordinated control the sensory and motor systems of the brain must be involved.
Because the pathways for all postural reactions are similar the interpretation of results is the same for all reactions. If hopping and placement are normal abnormalities are unlikely to be found in other reactions
Interpretation of paw placement deficits
tests sensation but also motor function required for response
Delay may occur due to lesion affecting ascending tract (ie signal not getting to brain)
But can also be seen due to weakness, peripheral neuropathy preventing normal response)
Interpretation of Hopping test
comparison of limb strength and coordination for contralateral limbs. Asymmetry is readily apparent so helps detect unilateral cerebral lesions where deficits are often mild but CONTRALATERAL to lesion. In spinal disease deficits are ipsilateral.
Delayed hopping may indicate a sensory or motor deficit to general proprioception
Poor initiation is seen with sensory deficits and poor follow through with motor
Increased tone in all limbs, normal to increased reflexes and proprioceptive deficits
Normal mentation and CN exam
C1-5 lesion, bilateral
Reduced withdrawal and tone in right forelimb, normal tone and withdrawal in left
Right forelimb delayed hopping and paw placement
Increased tone in right hind with normal patellar reflex. Reduced paw placement and hopping in right hind.
Normal reflexes and placement/hopping in left hind.
Right lateralising C6-T2 spinal lesion
Long strided hindlimb gait scuffing paws
Reduced hindlimb placement/proprioception but increased tone and normal reflexes
FL exam normal
T3-L3 lesion
Mild
Bilateral hindlimb paralysis with absent tone and sensation
Absent patellar reflexes and withdrawals absent
Absent anal sphincter tone
Severe L4-S3 lesion
Normal FL postural reactions but with rigid extension.
Flaccid paralysis of HLs with increased reflexes
Schiff Scherrington Phenomenon
–> severe T3-L3 lesion causing spinal shock resulting in disruption of normal UMN input to the HLs so appears as LMN
components of neurological exam
sensorium and behaviour,
posture and gait,
postural reactions,
muscle mass,
tone,
spinal reflexes and cutaneous sensation
AND cranial nerves.
What is the crossed extensor reflex
seen when performing the withdrawal response
Extension of the contralateral limb –> abnormal response indicating UMN lesion
Pathway of PLR
Light detected by retina
–> signal in optic nerve (both medial and lateral branches)
–> medial branch crosses to other side of brain
–> both synapse on occulomotor nerve nucleus in midbrain (both sides)
–> activation of parasympathetic fibres in occulomotor nerve
–> stimulation of the ciliary ganglion (parasympathetic input to iris)
–> pupil constriction in response to ACh
(sympathetic NS causes dilation) in both eyes
Does not assess vision but response to light which is a reflex not involving the cerebrum.
So can have blindness (ie signal not geting to forebrain with normal PLR if the lesion is caudal to CN3 nucleus)
What can cause both direct and consensual PLR to be absent in one eye
Lesion of the optic nerve or retina –> signal not getting into brain
Pathway of vision and subsequent menace response
Retina
–> optic nerve medial and lateral branches
–> optic chiasm
–> medial branch goes to contralateral lateral geniculate nucleus (and lateral branch goes to ipsilateral)
–> relay information to cortex via the optic tract
–> integration of visual stimuli from both eyes and mediates reactions
–> stimulates response via motor cortex
–> input to facial nerve nuclei in brainstem
–> LMN input to eyelids causing blink
What lesions can cause Menace deficit
Retinal or optic nerve as no visual input (ipsilateral)
Forebrain lesion will cause deficits on CONTRALATERAL side to lesion (due to decussation)
Optic tract lesion
After decussation so deficit is greatest on contralateral side.
Facial nerve neuropathy - will not blink but menace still present and vision normal
Cause of absent direct and consensual PLR in an eye with normal PLR direct and consensual in other eye
Occulomotor nerve lesion or parasympathetic innervation loss will be unilateral deficit on affected side (both with direct and indirect stimulation) but the opposite eye will have consensual constriction and direct constriction
How does vestibular system maintain balance and eye position
inner ear sensors detect movement in 3 dimensions (semicircular canals), rotary movement (ampulla) and linear acceleration (utricle)
–> in put to sensory afferent of vestibular nerve
–> peripheral vestibular ganglion (in internal acoustic meatus) –> efferents to brain
Pons and medulla
–> send signals to spinal extensors ipisilateral to the increased firing )
–> increased tone on side of increased firing
–> signals to CN III, IV VI nuclei to control eye movement
–> fast phase of movement is same direction as head movement.
Cerebellum also recieves input from vestibular efferent
–> projections that inhibit the action of afferents to the spinal cord negative feedback to prevent excessive tone)
Cause of nystagmus in vestibular disease
loss of input from affected side –> interpretation in brain as increased input from opposite side
–> fast phase nystagmus AWAY from lesion
