Neurological Examination Flashcards
List the clinical signs of Horner’s syndrome and the possible causes/pathogenesis
- Ptosis, miosis, protrusion of the 3rd eyelid, unilateral facial sweating, increased facial temperature and hyperaemia of the nasal and conjunctival membranes
- Causes: Perivascular injection, guttural pouch disease, trauma/infarction/haematoma/neoplasia (incl to cranial thoracic spinal cord or caudal cervical spinal cord), avulsion of the brachial plexus, damage to the sympathetic nerves in the vagosympathetic trunk (due to above causes), orbital/retrobulbar disease/injury.
- Pathogenesis: Loss of sympathetic innervation to the head (axons from UMN in the caudal hypothalamus, midbrain, pons, medulla oblongata descend in the cervical spinal cord to preganglionic neurons in the cranial thoracic spinal cord; from here they leave the cord and join the paravertebral sympathetic trunk, ascend the neck and synapse in the cranial cervical ganglion in the guttural pouch
List possible cranial nerves responsible for deviation in eye position
CN III, CN IV, CN VI, CN VIII (loss/damage to connection with the nuclei in the brainstem)
- Can occur with head trauma or mid-brain lesions (can be normal in foals)
List the clinical signs of damage to CN VIII
- Head tilt (poll towards the lesion/affected side)
- Disorientation (often)
- Proprioceptive deficits, asymmetric (may compensate visually with time) but preservation of strength*
- Falling &/or circling
- Horizontal nystagmus (initially; often only for 48-72hrs)
- Fast phase of nystagmus is away from the lesion if peripheral disease; if central, the nystagmus may be vertical, rotary or horizontal and may change with changing head position.
Describe the grades of ataxia (1-5 scale)
- Normal
- Requires careful examination to identify an abnormality
- Deficits are mild-moderate but obvious to most observers as soon as the horse begins to move
- Deficits are obvious and exaggerated by negotiation of a slope or head elevation
- May cause a horse to fall or nearly fall, often abnormal positioning while standing still
- Recumbent
or:
0 normal
1 needs provocation to see (eg circle)
2 present all times, visible to experienced observer only
3 obvious to anyone with eyes
4 falls spontaneously (ie when walking or standing, not when tightly circled or hopped etc)
5 recumbent
List the signs of LMN vs UMN dysfunction
LMN: Muscle atrophy, sensory loss, weakness, flaccid paralysis with hyporeflexia or areflexia, muscular hypotony.
UMN: Weakness, loss of voluntary motor function, however muscle tone may be increased and spinal reflexes may be normal to hyperactive - you can see spastic movement (due to reduced inhibition of extensor motor neurons)
List signs of cerebellar dysfunction
- Intention tremors, particularly of the head
- Failure to blink in bright light
- Lack of menace
- Ataxia/loss of coordination
- Dysmetria/hypermetria/jerky or stiff gait
- Intention tremors
- Truncal sway
- Vestibular signs or paradoxic vestibular syndrome (head tilt is away from lesion and nystagmus fast phase is towards the lesion - opposite to true vestibular disease)
Localise spinal cord disease based on affected region (thoracic limb, pelvic limb, both, tail tone, perineum etc)
Pelvic limb only: Caudal to T2 (T2/3-L3)
Thoracic limb primarily: C6-T2
Both: Typically pelvic limbs are one grade worse than thoracic limbs due to superficial location of pelvic limb spinocerebellar tracts in the SC; lesion is in the cervical spinal cord, cranial to C6
Reduced sensation and paresis of the tail & perineum +/- urinary and faecal incontinence/retention: (S3-S5) can produce hypalgesia, hypotonia and hyporeflexia of the tail, perineum and anus or total analgesia and paralysis.