*Vascular lesions on the Anterolateral system
Vascular supply to ALS originates from the arterial vasocorona via sulcal branches of anterior spinal artery
Lesions = patchy loss of pain, thermal, touch on contralateral side of body about 2 segments below lesion
*Anterolateral cordotomy
Complete loss of pain, thermal and touch sensations
*Spinal cord hemisection (Brown-Sequard): Contralateral
Loss of pain and thermal sensations all over body. Begins aout 2 segments below level of lesion (ALS damage)
*Spinal cord hemisection: Ipsilateral
Loss of discriminative tactile, vibratory and proprioception below lesion (posterior column damage).
Motor loss with paralysis of extremities
*Syringomyelia
Cysts in central gray matter that impinge the Anterior white commissure (which contains ALS fibers).
At c4-c5, bilateral loss of nondiscriminative tactile, pain and thermal sensation. Starts several segments below the lesion. Cape like distribution (shoulder to nipple level and arms - looks like a cape)
*Herpes zoster:
Viral DNA lays dormant in the nervous system. Virions travel down peripheral process and produce skin irritation in the dermatome. Diminished sense in affected areas. Postherpetic neuralgia
*Medullary syndrome:
Vascular lesions or tumors in the brainstem can impinge the ALS fibers and affect discriminative touch and nociception
*Lateral lesion for medullary syndrome
Wallenberg syndrome. Usually caused by vascular lesion to PICA which supplies the territory of the anterolateral system and the spinal trigeminal nucleus/tract
Contralateral loss of pain and temp with ipsilateral loss of pain and temp over face
*Medial lesion for medullary syndrome
Contralateral loss of discriminative touch and vibratory sense. Dissociated sensory loss
Pain and thermal sensations are intact
*Unilateral trigeminal nerve lesion:
Brainstem lesions destroy primary fibers in spinal trigeminal tract (descending tract) and secondary fibers in spinal lemniscus
Ipsilateral hemianalgesia of face and contralateral hemianalgesia of body
*Alternating analgesia/hemianesthesia
Brainstem lesions destroy primary fibers in spinal trigeminal tract (descending tract) and secondary fibers in spinal lemniscus
Ipsilateral hemianalgesia of face and contralateral hemianalgesia of body
*Alternating trigeminal hemiplegia:
Unilateral destruction of trigeminal nerve and CST in pons
Ipsilateral anesthesia, paralysis and contralateral spastic hemiplegia
*Damage to trigeminal nerve or central nuclei:
Primary deficits include ipsilateral loss of pain, thermal or tactile sensations of face and scalp, oral cavity and teeth. Ipsilateral paralysis of mastication muscles
Also loss of afferent limb of corneal reflex
*Vascular lesions on the Anterolateral system
Vascular supply to ALS originates from the arterial vasocorona via sulcal branches of anterior spinal artery
Lesions = patchy loss of pain, thermal, touch on contralateral side of body about 2 segments below lesion
Lower motor neuron lesions usually presents with ….
Flaccid paralysis, wasting, hyporeflexia, hypotonia and fasciculations (muscle twitches)
Upper motor neuron signs
Loss of the direct corticospinal tract and loss of regulation from the indirect brainstem motor control pathways
Symptoms of upper motor neuron signs:
CST problems:
Indirect pathways modulation problems:
Loss of distal extremity strength Babinski sign (inverted plantar reflex
Hypertonia (spastic or rigid)
Hyperreflexia (clonus)
Clasp knife phenomenon and spasticity
Pronator drift)
Clues in LMN lesions
Clinical signs ipsilateral to lesion
Decorticate posture:
bent arms, clenched fists, and legs held out straight, feet extended and inverted
Lesion above the level of the red nucleus
Decerebrate posture:
Upper extremity in pronation and extension and lower extremity in extension
Complete transection of spinal cord
All sensation 1 or 2 levels below lesion lost due to overlap of dermatomes Incontinence Spinal shock (loss of tendon reflexes) UMN signs at levels below the lesion LMN signs at the level of lesion
Hemisection of spinal cord (Brown Sequard)
Pain and temp loss from contralateral side of body and loss of discriminative touch and proprioception on the ipsilateral side
LMN signs at level of lesion (flaccid paralysis)
UMN signs on ipsilateral side of lesion
Syringomyelia
Cysts in spinal cord. Affects pain and temp sensation first due to impingement of the anterior white commissure. Cape pattern sensation loss.
Motor also lost (LMN signs if ventral horn is affected or UMN signs if lateral corticospinal tract is affected)
Anterior cord syndrome
Damage to anterior spinal cord (usually due to spinal cord infarction, herniation or myelopathy
Central cord syndrome
Central spinal cord damage usually due to cervical hyperextension
Central Seven Palsy
Corticobulbar tract lesion involving CN VII. Upper face controlled equally by both hemispheres. Lower face is controlled by contralateral hemisphere.
Lesions rostral to CN VII nucleus results in muscle drooping on corner of mouth (contralateral side of lesion)
Bell’s palsy
Ipsilateral flaccid paralysis of upper and lower face
Spastic cerebral palsy
Spastic movement dysfunction.
Paresis, abnormal reflexes, abnormal postural coordination
Amytrophic lateral sclerosis (ALS)
UMNs and LMNs destruction. UMN and LMN signs
CN involvement results in difficulty breathing, swallowing or speaking
Polyneuropathy
Progress distal to proximal due to impaired axonal transport or demyelization. Affects sensory, motor and autonomic functions
Nature of cerebellar lesions.
Specific to the cerebellum (problem with afferents and efferents)
Voluntary jerky, inaccurate movements, wide based gait
Ataxia:
Specific to the cerebellum (problem with afferents and efferents)
Voluntary jerky, inaccurate movements, wide based gait
Lesions of the vestibulocerebellum
Disrupts the integration of the vestibular system and flocculonodular lobe.
Nystagmus (beating of the eyes), truncal ataxia and truncal instability
Truncal ataxia
Truncal instability
can’t maintain sitting or balance. wide spaced gait
Cannot stand still/rocking, can’t tandem walk
Spinocerebellum lesions
Disrupts the connections between the cutaneous and proprioceptive tracts from the spinal cord to vermis region
Wide base gait and truncal ataxia
Damage to vestibulocerebellum and spinocerebullum generally result in…
Midline ataxia
Midline ataxia
Caused by vestibulo and spinocerebellar disease
Truncal instability. Tremor of trunk (titubation) and gait ataxia
Lesions of the cerebrocerebellum
Dysarthria: slurred speech (difficulty articulating)
Gait ataxia - tend to fall toward side of lesion
Limb ataxia due to cerebrocerebellar damage:
Dysdiadochokinesia
Dysmetria
Action tremor
- cannot rapidly alternate movements
- cannot move an intended distance
- shaking of limb during voluntary movement
Appendicular ataxia
Cerebellar hemisphere dysfunction Scanning dysarthria (speech ataxia), hypotonia, dysmetria, dysdiadochokinesia, decomposition of movement
Cerebellar ataxia
Positive romberg test - Unable to stand with feet together (with or without eyes open)
Normal vibratory, proprioception and ankle reflex
Sensory ataxia:
Positive Romberg test - Can stand with feet together and eyes open, but not when closed.
Abnormal vibratory, proprioception and ankle reflex