Limited Damage
- although damage may be severe, deficits are limited to the structures innervated by the particular affected nerve(s). (Deficits may be widespread in cases of polyneuritis//polyneuropathy.)
Flaccid Paralysis
- paralysis is flaccid and includes areflexia of muscles innervated by the particular nerve(s)
Neurogenic Muscle Atrophy
- atrophy of muscles innervated by the particular nerve(s) is severe and relatively rapid (evident by two weeks)
Skin Anesthesia/Analgesia
- anesthesia of skin fields innervated by cutaneous branches of affected nerve(s)
Note:
There is a resemblence between neuropathy syndromes and syndromes produced by CNS lower motor neuron damage and diseases of neuromuscular junctions.
Damage affects sacral and caudal spinal segments/roots, which innervate the pelvis & tail.
- tail flaccid paralysis, muscle atrophy, and skin anesthesia
- perineum anesthesia, including the anal region
- fecal and urinary incontinence due to sphincter paralysis
- enlarged atonic bladder with urine overflow
Damage affects spinal segments/roots L4 - S1, which innervate the pelvic limb.
segmental & LMN deficits:
- pelvic limb muscles exhibit flaccid paralysis, areflexia, and muscle atrophy
- pelvic limb skin exhibts areas of anesthesia
tract & UMN deficits:
- tail voluntary paralysis and loss of conscious sensation
- voluntary incontinence; incomplete urination with residual urine retention
Damage affects spinal segments/roots T3 - L3, which innervate the trunk.
segmental & LMN deficits:
- absence of cutaneous trunci reflex caudal to the lesion; cutaneous hyper/hypo-esthesia at lesion level; (LMN clinical signs are difficult to detect)
tract & UMN deficits:
- voluntary paralysis and loss of conscious sensation in pelvic limb & tail
- pelvic limb:
deficits of postural reactions (e.g., proprioceptive positioning, hopping, hemiwalking, etc.);
extensor muscle hypertonus may be present (pending the nature of tract damage);
spinal reflexes are present, including abnormal crossed-extension.
- voluntary incontinence; incomplete urination with residual urine retention (detrusor-sphincter dyssynergy)
Damage affects spinal segments/roots C6 - T2, the cervical enlargement which innervates the thoracic limb.
segmental & LMN deficits:
- thoracic limb muscles may exhibit flaccid paralysis, areflexia, and muscle atrophy
- thoracic limb skin may exhibit areas of anesthesia
- cutaneous trunci reflex may be absent due to damage to lateral thoracic nerve neurons
tract & UMN deficits:
- voluntary paralysis and loss of conscious sensation in trunk, pelvic limb & tail
- pelvic limb: ataxia; deficits of postural reactions (e.g., proprioceptive positioning, hopping, hemiwalking, etc.); extensor muscle hypertonus may be present; spinal reflexes are present, including abnormal crossed-extension;
- voluntary incontinence; incomplete urination with residual urine retention (detrusor-sphincter dyssynergy)
Damage affects spinal segments/roots C1 - C5, which innervate the neck.
segmental & LMN deficits:
- cutaneous hyper/hypo-esthesia at lesion level; (LMN clinical signs are difficult to detect)
tract & UMN deficits:
- voluntary paralysis and loss of conscious sensation caudal to the neck
- thoracic & pelvic limbs: ataxia; deficits of postural reactions (e.g., proprioceptive positioning, hopping, hemiwalking, etc.); extensor muscle hypertonus may be present; spinal reflexes are present, including abnormal crossed-extension;
- voluntary incontinence; incomplete urination with residual urine retention (detrusor-sphincter dyssynergy)
Damage to cranial nerves can indicate the level(s) of a brainstem lesion(s):
- trigeminal nerve [pons]: loss of face sensation & paralysis of muscles of mastication
- abducent nerve [rostral medulla]: medial strabismus (the nerve runs to the orbital fissure)
- facial nerve [medulla]: paralysis of facial expression,e.g., drooped lips
- vestibulocochlear nerve [medulla]: vestibular syndrome; unilateral deafness
- glossopharyngeal nerve [rostral medulla]: impaired gag reflexes and pharyngeal sensation
- vagus nerve [medulla]: paralysis of pharynx and larynx (gag reflexes & voice change)
- hypoglossal nerve [caudal medulla]: tongue paralysis, atrophy & deviation toward lesion side
Damage to descending tracts that originate and/or pass through the hindbrain:
- pontine reticulospinal & lateral vestibulospinal: ipsilateral falling (extensor hypotonus)
- rubrospinal tract: ipsilateral joint flexion paralysis of thoracic & pelvic limbs
- pyramidal tract: contralateral weakness of manus & pes, especially navigating steps
Damage to autonomic centers could impact respiration, heart rate, etc.
Vestibular syndromes can result from damage affecting the labyrinth, vestibular nerve, vestibular nuclei and/or cerebellum
Vestibular syndromes reflect the brain’s response to a right/left imbalance of vestibular input, the imbalance due to a lesion instead of head acceleration
The direction of the clinical signs reveals which side is damaged (decreased neural activity); the severity of the clinical signs reflects the severity of the lesion (extent of the imbalance)
Clinical signs comprising the vestibular syndrome include:
- head tilt [down ear toward the lesioned side]
- stumbling, falling, rolling [toward the lesioned side]
- nystagmus [slow phase toward the lesioned side]
(nystagmus in a vertical direction, as opposed to horizontal, is said to indicate a brain lesion location).
Cerebellar damage generally causes excess muscle tone & exaggerated movement.
Clinical signs associate with a cerebellar syndrome include:
- wide based stance (required for to maintain balance during standing)
- ataxic gait (limb foot-fall placement is inconsistent and malpositioned)
- hypermetric gait (limbs are protracted too high and slammed down too hard)
- intention tremor (e.g., head tremor, exhibited when the head is not resting on the ground)
- body swaying (another manifestation of tremor)
- menace response deficiency (elicited by threatening gesture). Judgment of rate of changing distance for approaching objects is impaired.
Destructive lesions of the midbrain would be expected to produce:
- paresis/paralysis of the contralateral limbs due to red nucleus damage (contralateral deficits occur when the damage is rostral to the rubrospinal tract decussation in the caudal midbrain); damage to corticospinal axons in the crus cerebri would impact the contralateral manus/pes- lateral strabismus and loss of the pupillary light reflex would result from oculomotor nucleus/nerve damage
- trochlear nucleus/nerve damage would impair (dorsal) eye rotation toward the nose
- impaired orientation of the head, eyes & ears toward a sudden visual (rostral colliculus) or auditory (caudal colliculus) stimulus
- coma may result from destruction of the reticular activating system (which generates background excitation for the cerebral cortex)
Destructive lesions of the diencephalon would be expected to produce:
- crying behavior (apparently due to pain) has been observed with thalamic infarct lesions- loss of conscious sensation (information is relayed to the neocortex through the thalamus)
- blindness:
optic nerve damage: ipsilateral complete blindness & absent pupillary reflex to ipsilateral light
optic tract or lateral geniculate nucleus damage: contralateral sides of visual fields are blind for both eyes
- endocrine disorders, due to hypothalamic & pituitary damage
- autonomic disorders related to eating, drinking, temperature regulation, circadian rhythms, etc., due to hypothalamus damage
Destructive lesions of the cerebrum could produce:
- mental impairment:
depressed alertness & interaction with surroundings
depressed intelligence & deficient learning/learned behavior (including house-training)
- inability to perform goal-directed behavior (task focusing, short term memory, ignoring distractions, controlling emotions) as a result of damage to the prefrontal cortex of the frontal lobe
- neglect syndrome (parts of a patient's own body are regarded as foreign by the patient)
- seizures
- mood alteration (such as uncharacteristic aggression or docility) .
Note: Lesions in one cerebral hemisphere produce contralateral motor/sensory deficits.