Spastic spinal paralysis

It is mainly used in the treatment of spasticity in multiple sclerosis, spastic spinal paralysis etc. It is also used in the treatment of trigeminal neuralgia. 

Generally a much more limited increase in serum creatine kinase is encountered in the adult form of muscular dystrophy and in myotonic dystrophy. It is normally raised in untreated cases of polymyositis, and the level may be very high. Typical data are provided by Pearce et al [113] and other workers. It was at one time considered that little or no rise in serum creatine kinase occurred in muscle diseases of recognized neurogenic origin, but modest increases have been recorded in Kugelberg-Welander disease and spastic spinal paralysis [115] and in motor neurone disease [116]. Elevated values may occur also in hyperkalaemic and hypokalaemic myopathies [117, 118]. 

Motor neuron disease is characterized clinically by weakness, muscle atrophy and spasticity. This illness, often termed Lou Gehrig s disease in the United States, is the most common adult-onset form of MND with a prevalence of approximately 2-3 per 100,000 people [1-3,10, 25, 28]. Each year in the United States, in excess of 5,000 people are diagnosed with ALS. In parts of the United Kingdom, 1 in =500 deaths are attributed to some form of MND. The principal clinical signs of ALS include progressive limb weakness, which may be symmetrical or asymmetrical atrophy of appendicular, bulbar and respiratory muscles and spasticity [1,2,26,28]. The paralysis/muscle atrophy and spasticity are the result of degeneration of motor neurons in the spinal cord/brain stem and motor cortex respectively. The onset of this illness is typically in the fifth or sixth decade of life affected individuals usually... 

A potential source of cyanide poisoning is cassava, a starch from the root of Manihot esculenta, used as food in much of Africa. The root contains cyanogenic linamarin, which is normally removed in processing the root for food. Widespread cases of a spinal cord disorder called konzo and characterized by spastic paralysis have been attributed to ingestion of linamarin from inadequately... 

The blockade of inhibitory synapses at the spinal cord impairs the neuronal circuitry that controls voluntary muscle contraction, thereby causing the spastic paralysis characteristic of tetanus (Simpson, 1989). 

Tetanus toxin poisoning produces tetanus, i.e. muscle contractions resulting in spastic paralysis. In contrast, Botulinum neurotoxins cause botulism, which is characterized by flaccid paralysis. This difference reflects differences in the anatomical level of action of these toxins. TeTx acts primarily on the CNS where it blocks exocytosis from inhibitory glycinergic synapses in the spinal cord. Loss of inhibitory control results in motoneuron firing. BoNTs act primarily in the periphery where they inhibit acetylcholine release at the neuromuscular junctions. 

Tetanus toxin. Protein neurotoxin produced by the bacterium Lostridium tetani. Blocks inhibitory synapses in the spinal cord spastic paralysis, followed by block of ACh release in periphery, resulting in flaccid paralysis. 

By contrast, tetanus toxin primarily has a central action it is transported in retrograde fashion up the motor neuron to its soma in the spinal cord. From there the toxin migrates to inhibitory neurons that synapse with the motor neuron and blocks exocytosis in the inhibitory neuron. The block of release of inhibitory transmitter gives rise to tetanus or spastic paralysis. The toxin from the venom of black widow spiders (a-latrotoxin) binds to neurexins, transmembrane proteins that reside on the nerve terminal membrane, resulting in massive synaptic vesicle exocytosis. 

---