The iron from blood also reduces the activity of an enzyme called nitric oxide synthase, another factor thought to contribute to PTE.After TBI, abnormalities exist in the release of neurotransmitters, chemicals used by brain cells to communicate with each other; these abnormalities may play a role in the development of PTE. TBI may lead to the excessive release of glutamate and other excitatory neurotransmitters (those that stimulate brain cells and increase the likelihood that they will fire). This excessive glutamate release can lead to excitotoxicity, damage to brain cells through overactivation of the biochemical receptors that bind and respond to excitatory neurotransmitters. Overactivation of glutamate receptors damages neurons; for example it leads to the formation of free radicals. Excitotoxicity is a possible factor in the development of PTE; it may lead to the formation of a chronic epileptogenic focus. An epileptic focus is the part of the brain from which epileptic discharges originate.In addition to chemical changes in cells, structural changes that lead to epilepsy may occur in the brain. Seizures that occur shortly after TBI can reorganize neural networks and cause seizures to occur repeatedly and spontaneously later on. The kindling hypothesis suggests that new neural connections are formed in the brain and cause an increase in excitability. The word kindling is a metaphor: the way the brains response to stimuli increases over repeated exposures is similar to the way small burning twigs can produce a large fire. This reorganization of neural networks may make them more excitable.
Klumpkes paralysis is a variety of partial palsy of the lower roots of the brachial plexus. The brachial plexus is a network of spinal nerves that originates in the back of the neck, extends through the axilla (armpit), and gives rise to nerves to the upper limb. The paralytic condition is named after Augusta Déjerine-Klumpke. Signs and symptoms
Symptoms include intrinsic minus hand deformity, paralysis of intrinsic hand muscles, and C8/T1 Dermatome distribution numbness. Involvement of T1 may result in Horners syndrome, with ptosis, and miosis. Weakness or lack of ability to use specific muscles of the shoulder or arm. It can be contrasted to Erb-Duchennes palsy, which affects C5 and C6. Cause
Klumpkes paralysis is a form of paralysis involving the muscles of the forearm and hand, resulting from a brachial plexus injury in which the eighth cervical (C8) and first thoracic (T1) nerves are injured either before or after they have joined to form the lower trunk. The subsequent paralysis affects, principally, the intrinsic muscles of the hand (notably the interossei, thenar and hypothenar muscles) and the flexors of the wrist and fingers (notably flexor carpi ulnaris and ulnar half of the flexor digitorum profundus). The classic presentation of Klumpkes palsy is the “claw hand” where the forearm is supinated, the wrist extended and the fingers flexed. If Horner syndrome is present, there is miosis (constriction of the pupils) in the affected eye.The injury can result from difficulties in childbirth. The most common aetiological mechanism is caused by a traumatic vaginal delivery.