Disease relevance of Paraparesis

• OBJECTIVES: To investigate whether cognitive decline is part of the phenotype of SPG4-linked hereditary spastic paraparesis (HSP) and to determine whether cognitive changes are present in haplotype carriers before the onset of paraparesis [1].
• Ketoconazole is particularly valuable when a prompt therapeutic response is needed and orchiectomy is contraindicated because of bleeding diathesis (as in disseminated intravascular coagulation), delay in histological confirmation (as in acute paraparesis/paraplegia) or patient reluctance to undergo castration [2].
• For example, treatment with methylprednisolone more than doubled the probability that patients would convert from quadriplegia or paraplegia to quadriparesis or paraparesis, analgesia to hypalgesia, and anesthesia to hypesthesia [3].
• A patient with active giant cell arteritis developed paraparesis and dissociated sensory loss due to infarction in the anterior spinal artery territory at the level of T12 [4].
• The role of aging, genetic background, HTLV-1 infection and other factors on the development of HAM/TSP-like paraparesis in rats are discussed [5].

Psychiatry related information on Paraparesis

• Electromyographic reaction times (EMG-RTs) of the right knee extension were examined in eight normal subjects and eight patients with paraparesis under three conditions; during passive knee flexion (PFLX), passive extension (PEXT) and no passive movements (STAT) [6].
• Clinical signs of disease included disorientation and truncal ataxia that rapidly progressed to hemiparesis or paraparesis [7].

High impact information on Paraparesis

• Changes in the excitability of the soleus H-reflex are were studied after oral administration of L-acetylcarnitine, a cholinomimetic substance, in eight healthy control subjects and 23 spastic patients presenting with slowly progressive paraparesis (n = 10), a cord lesion (n = 9) and a cerebral lesion (n = 4) [8].
• Ganciclovir therapy, 5-10 mg/kg per day, instituted 3-6.5 weeks after onset of symptoms, was ineffective in four patients with severe paraparesis [9].
• Comparison of the mutation-positive group with the SPG4-excluded group revealed an older age at onset (p = 0.03), more disability (p = 0.001), more rapidly progressive paraparesis (p = 0.044), and more cognitive impairment (p = 0.024) among affected individuals with SPAST mutations, not confounded by disease duration [10].
• Six of the eight (75%) WKA rats injected with MT-2 cells showed HAM/TSP-like paraparesis at 108 weeks of age [11].
• After cyclophosphamide and glucocorticoid therapy, both her acute deficits and chronic paraparesis improved [12].

Chemical compound and disease context of Paraparesis

• Dexamethasone treatment commenced after evident paraparesis accelerated recovery, but did not influence SPM density [13].
• Moderate trauma, leading to transient paraparesis, resulted in a transient rise of glutamate and taurine [14].
• No signs of early neurologic injury developed in any of the patients in the intrathecal papaverine group, although delayed paraparesis developed in one of the patients (9%; 70% confidence limits = 1% to 28%) [15].
• GABA agonists did not improve the paraparesis [16].
• Flaccid paraparesis following obstetrical epidural anesthesia: possible role of benzyl alcohol [17].

Anatomical context of Paraparesis

• The affected animals developed clinical signs of a sensory axonopathy consisting of hindlimb spasticity and ataxia as early as 3 weeks of age, with progression to paraparesis and severe morbidity by 6 months of age [18].
• The efficacy of three different regimens of the 21-aminosteroid U74006F in counteracting the neurological damage after spinal cord compression causing paraparesis in rats was investigated [19].
• The paraparesis progressed rapidly to extensor paralysis with subsequent involvement of the forelimbs with flexor paralysis [20].
• Six weeks later, the infant experienced a mild paraparesis with a palsy of the left sixth cranial nerve, which disappeared following steroid therapy [21].
• Case report 384: Paraparesis from cauda equina compression due to disc herniation of L4-L5, in a patient with ossification of the posterior longitudinal ligament (OPLL) at L4-L5 and C4-C5 [22].

Gene context of Paraparesis

• To exploit the fact that IL-2Rs are present on abnormal T cells in patients with tropical parasitic paraparesis/HTLV-I-associated myelopathy (TSP/HAM) and ATL but not on normal resting cells, different forms of IL-2R-directed therapy have been initiated [23].
• We report the case of a middle-aged Englishman who presented with complaints of intermittent paraparesis due to OPLL at the T5-T6 level in his thoracic spine [24].
• Paraparesis in hereditary multiple exostoses: case report [25].
• The most common findings were a discrete sensory level in 5 patients, hyperreflexia in 5 patients, and paraparesis or paraplegia in 5 patients [26].
• We now describe a 2-generation family with ODDD and progressive paraparesis associated with leukodystrophic changes documented by MRI [27].

Analytical, diagnostic and therapeutic context of Paraparesis

• Radiotherapy and bromocriptine in extreme doses (140 mg daily) together with an antiestrogen were not able to improve the neurological deficits (paraparesis) and to lower the PRL levels [28].

References