Spinal Pathology

Recovery of function in the spinal cord. Traumatic spinal injury, the consequences of transection. Period of areflexia and hypotonus and flaccid paralysis. Period of hyperreflexia and hypertonus in which nerve-muscle transmission is facilitated abnormally. State of moderate hyperreflexia and increased tonus (spastic paralysis). Re-establishment of autonomic control of smooth muscle via postganglionic sympathetic neurons allows for the establishment of a reflex bowel and bladder. Postural reflexes in spinal humans are remarkably intact yet entirely isolated from voluntary control; Ia and Ib systems moderate motoneuron discharge in spinal humans, extensors are predominantly activates. Spinal lesions that interrupt vestibulospinal and reticulospinal tracts impair posture and locomotion. Can cerebellar influences reach motoneurons in the spinally hemisected human? The functional reorganization of the nervous system illustrates plasticity in somatic sensory cortex, representation after peripheral manipulation. Somatotopy of digit representation in area 3 in SI is plastic, responsive to experience and surprisingly flexible

Degeneration and regeneration in the nervous system occurs in a system, anterograde changes from cell body to axon and retrograde changes from axon or axon terminals to the cell body. Denervation supersensitivity facilitates residual cutaneous and neuromuscular responsiveness after peripheral damage; this causes a transient hyperreflexia

Responses of nerve cells to damage, defining trauma. Alterations in intra and extracellular pH affect neuronal discharge profoundly. A coma, in which decreased permeability hyperpolarizes the neuron and leads to progressive inexcitability. Epileptic discharge and status epilepticus; Jacksonian seizures; petit mal seizures. Ischemia and the reversibility of trauma. Development constraints, protein malnourishment permanently impairs myelination and reduces conduction velocity. Effects of environmental toxins on neurological integrity; mercury poisoning. The locus and severity of axotomy is the primary factor in neuronal survival. Bi-directional degenerative changes are the consequence of severe damage. Cell body and the signals for chromatolysis, axon terminals retreat or regenerate, postsynaptic receptors are affected severely by axotomy, and their density and spatial distribution can be altered, leading to denervation supersensitivity or hyperreflexia. The factors responsible for recovery or degeneration are the residual volume of the neuron or axon and the patency of afferent connectivity and of synaptic activity. Degeneration in the nervous system, retrograde changes affect neuronal modulation, transport and connectivity, anterograde changes and gliotic response can impair/impede outgrowth and/or reduce the diameter of the regenerating axon, lowering conduction velocity in the fiber. Transsynaptic changes are critical in learning, memory, recovery from damage and plasticity of neuronal organization.

Recovery of Function

*LH*
acoustic reflex - auditory/facial nerve reflex arc that pulls the acoustic muscle tight dampening high amplitude sounds; pulls on the incus, malleus and stapes to dampen sound that's high in amplitude
babinski reflex - elicited by scraping sole of the foot causing dorsiflexion (pulling up) of toes - from lesion of corticospinal tract; SDR
patellar reflex - elicited by tapping patellar tendon causing kicking motion (contraction of upper leg extensors)
romberg sign - patients that lose joint position sensation will tend to fall when they close their eyes while standing still with their feet close together

• tabes dorsalis
• helps differentiate between peripheral and cerebellar ataxia (inability to coordinate voluntary muscle movements)

hoffman sign - sudden flicking of the nail of the index, middle or ring fingers produces flexion of the thumb and some other fingers (digital reflex)

• seen in cervical myelophathy

l'hermitte's sign - weakness in all limbs when patient flexes head forward (transient dyesthesia)

• seen in cervical cord injuries or cord degeneration

tinel's sign - lightly banging nerve (precussion) causes a tingling or pins and needles sensation

• carpal tunnel syndrom will cause tingling or thumb, index finger and middle finger

brown sequard - ipsilateral paralysis, loss of discriminitory joint sensation, contralateral loss of pain and temperature sensation

• caused by damage to half of the spinal cord

horner's - sinking of eyeball, ptosis or upper eyelid, elevation of lower lid constriction of pupil, narrowing of palpebral fissure, flushing of affected side of face

• caused by paralysis of cervical sympathetic nerves

tourettes - brain disorder causing facial twitching, involuntary outbursts of profanity and other random symptoms

trieminal neuralgia - (tic doulooureaux) - severe facial pain caused by compression of the trigeminal nerve by a blood vessel (SCA) * do not confuse for hemi - facial spasm * trigeminal not facial

arnold-chiari malformation - malpositioned brainstem or cerebellum causing stenosis of the brainstem at the foramen magnum; can maybe end up with trapezius weakness from the spinal accessory

bell's palsy - facial muscle paralysis due to facial nerve dysfunction

• caused by lesion along the facial nerve in the brainstem or commonly caused by infection and inflammation along the facial nerve
• often where the nerve exits the foramen
  

Multple sclerosis - demyelinating plaques affecting the central nervous tracts, progressive degenerative disorder
charcot-marie-tooth - widespread demyelination causing peripheral neuropathy

• vascular tome
• spinal cord injury protocol
• steroids increase blood pressure

friedrich's ataxia - results in abnormal or absent SSEP's, progressive disorder affecting large myelinated fibers in the nervous system

• causes a loss of balance and coordination

myesthenia gravis - muscle weakness caused by insufficient production of acetylcholinesterase

• leaves acetylcholine at the synapse does not get re-uptaken into the synaptic bouton
  

amyotrophic lateral sclerosis - (ALS or lou gherig's diesease) - progressive paralysis caused by progressive nervous disorder which attacks motor fibers

thoracic outlet syndrom - compression of the brachial plexus nerve trunks, characterized by pain in the arms, parasthesia of the fingers, vasomotor symptoms, and weakness with wasting of the small muscles of the hand. often caused by compression from an extra rib or abnormally placed muscle