The appearance of the patient is like a man being confined in a barrel.1 This rare syndrome is associated with cerebral hypoperfusion due to border zone infarcts that are generally present between the anterior and middle cerebral artery irrigation areas.2 In addition to many cerebral lesions with different natural characteristics that cause the upper limb-related fibres of the pyramidal
corticospinal tract to be injured, cervical spinal cord lesions and peripheral nerve diseases may also be present with this disease.3 Herein we presented a patient with MIBS which was due to bilateral brachial plexopathy caused by recurrent microtrauma.
Meanwhile, our previous cross-sectional study demonstrated that the GM volume of the whole brain did not significantly differ between ALS patients and healthy controls (HCs),[9] though FA in the bilateral
corticospinal tract and corpus callosum was significantly lower in the ALS group than in the HC group,[18] indicating that the microstructural involvement of WM was more prominent than GM damage in ALS patients at baseline.
Abnormalities in axon guidance and the
corticospinal tract (CST) are observed in the absence of ephrin or DCC genes in knock-out animal studies (17, 18).
Axon diameter and intra-axonal volume fraction of the
corticospinal tract in idiopathic normal pressure hydrocephalus measured by Q-Space imaging.
MRI also showed hyperintensity of the globus pallidus, thalamus, dorsal aspect of the brain stem,
corticospinal tract, and cerebellum.
In a previous study, researchers demonstrated that virus-mediated expression of osteopontin and insulin-like growth factor (IGF1) promoted the regrowth of brain-derived
corticospinal tract (CST) axons and functional recovery of CST-dependent motor function following an incomplete SCI lesion.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by upper motor neuron,
corticospinal tract, and lower motor neuron involvement.
In turn, this could lead to decreased activity of the striatum, which inhibits the inhibitory output from the BG network to the thalamus modulating the activity of the
corticospinal tract [2].
The integrity of the
corticospinal tract also predicts motor function potential [25, 40, 41].
Animal studies have revealed that a hierarchy of spinal and supraspinal plasticity (from the cerebellum to sensorimotor cortex to
corticospinal tract to spinal cord) is involved in inducing and maintaining the operant conditioning-induced change in the evoked response [31,32].
Neurologic sequelae from vitamin [B.sub.12] deficiency include paresthesias, peripheral neuropathy, and demyelination of the
corticospinal tract and dorsal columns [subacute combined degeneration of the spinal cord (SCD)].
Picht, "A new approach for
corticospinal tract reconstruction based on navigated transcranial stimulation and standardized fractional anisotropy values," NeuroImage, vol.