Neurectomy of C2 for the Treatment of Occipital Neuralgia: Case Report

Occipital neuralgia (ON) is an uncommon cause of headache, and it is characterized by a stabbing paroxysmal pain that radiates to the occipital region. The present study includes a review of the literature and a case report. The etiology of this pathology can vary from traumas, infections, compressions of nerves or vertebrae, skull base surgeries, to degenerative changes and congenital anomalies. However, most of the time, the etiology is considered idiopathic. The diagnosis is essentially clinical. However, it is crucial that other types of primary headache are excluded. The treatment for ON may be based on nerve blocks, medications or surgeries. Neurectomy of the second spinal nerve is among the surgical techniques available.

Cdk5-Dependent Phosphorylation of CaV3.2 T-Type Channels: Possible Role in Nerve Ligation-Induced Neuropathic Allodynia and the Compound Action Potential in Primary Afferent C Fibers.

Voltage-gated T-type Ca2+ (CaV3) channels regulate diverse physiological events, including neuronal excitability, and have been linked to several pathological conditions such as absence epilepsy, cardiovascular diseases, and neuropathic pain. It is also acknowledged that calcium/calmodulin-dependent protein kinase II and protein kinases A and C regulate the activity of T-type channels. Interestingly, peripheral nerve injury induces tactile allodynia and upregulates CaV3.2 channels and cyclin-dependent kinase 5 (Cdk5) in dorsal root ganglia (DRG) and spinal dorsal horn. Here, we report that recombinant CaV3.2 channels expressed in HEK293 cells are regulatory targets of Cdk5. Site-directed mutagenesis showed that the relevant sites for this regulation are residues S561 and S1987. We also found that Cdk5 may regulate CaV3.2 channel functional expression in rats with mechanical allodynia induced by spinal nerve ligation (SNL). Consequently, the Cdk5 inhibitor olomoucine affected the compound action potential recorded in the spinal nerves, as well as the paw withdrawal threshold. Likewise, Cdk5 expression was upregulated after SNL in the DRG. These findings unveil a novel mechanism for how phosphorylation may regulate CaV3.2 channels and suggest that increased channel activity by Cdk5-mediated phosphorylation after SNL contributes nerve injury-induced tactile allodynia.SIGNIFICANCE STATEMENT Neuropathic pain is a current public health challenge. It can develop as a result of injury or nerve illness. It is acknowledged that the expression of various ion channels can be altered in neuropathic pain, including T-type Ca2+ channels that are expressed in sensory neurons, where they play a role in the regulation of cellular excitability. The present work shows that the exacerbated expression of Cdk5 in a preclinical model of neuropathic pain increases the functional expression of CaV3.2 channels. This finding is relevant for the understanding of the molecular pathophysiology of the disease. Additionally, this work may have a substantial translational impact, since it describes a novel molecular pathway that could represent an interesting therapeutic alternative for neuropathic pain.

Blockade of anoctamin-1 in injured and uninjured nerves reduces neuropathic pain.

The aim of this study was to determine the participation of anoctamin-1 in 2 models of neuropathic pain in rats (L5/L6 spinal nerve ligation [SNL] and L5 spinal nerve transection [SNT]). SNL and SNT diminished withdrawal threshold in rats. Moreover, SNL up-regulated anoctamin-1 protein expression in injured L5 and uninjured L4 DRG whereas that it enhanced activating transcription factor 3 (ATF-3) and caspase-3 expression only in injured L5 DRG. In marked contrast, SNT enhanced ATF-3 and caspase-3, but not anoctamin-1, expression in injured L5 DRG but it did not modify anoctamin-1, ATF-3 nor caspase-3 expression in uninjured L4 DRG. Accordingly, repeated (3 times) intrathecal injection of the anoctamin-1 blocker T16Ainh-A01 (0.1-1 µg) or MONNA (1-10 µg) partially reverted SNL-induced mechanical allodynia in a dose-dependent manner. In contrast, anoctamin-1 blockers only produced a modest effect in SNT-induced mechanical allodynia. Interestingly, intrathecal injection of T16Ainh-A01 (1 µg) or MONNA (10 µg) prevented SNL-induced up-regulation of anoctamin-1, ATF-3 and caspase-3 in injured L5 DRG. Repeated intrathecal injection of T16Ainh-A01 or MONNA also reduced SNT-induced up-regulation of ATF-3 in injured L5 DRG. In contrast, T16Ainh-A01 and MONNA did not affect SNT-induced up-regulation of caspase-3 expression in L5 DRG. Likewise, gabapentin (100 µg) diminished SNL-induced up-regulation of anoctamin-1, ATF-3 and caspase-3 expression in injured L5 DRG. These data suggest that spinal anoctamin-1 in injured and uninjured DRG participates in the maintenance of neuropathic pain in rats. Our data also indicate that expression of anoctamin-1 in DRG is differentially regulated depending on the neuropathic pain model.

Neurorrafia do nervo espinal acessorio apos esvaziamento cervical radical para reabilitacao funcional do ombro / Post radical neck dissection spinal acessory nerve grafting for shoulder functional rehabilitation

O esvaziamento cervical radical e de indicaçao frequente na indicaçao terapeutica do cancer da cabeça e pescoço. A dor, disfunçao e quedado ombro sao as principais consequencias desse tratamento e apresentam importante papel na reintegraçao social e ocupacional dos pacientes. De fevereiro del980 a abril de l987 no Serviço de Cabeça e Pescoço do Hospital Heliopolis- SaoPaulo, foram realizados 91 esvaziamentos cervicais radicais modificados pela dissecçao,secçao e sutura do nervo espinal,com intuito de minimizar os efeitos resultantes da disfunçao da musculatura da cintura escapular.Sao apresentados atecnica utilizada e os resultados quanto a reinervaçao do musculo trapezio,que atinge de 50% a 80% da funçao normal(71%dos casos) em intervalos variaveis de tempo entre 3 e 12 meses.Trata-se de uma intervençao que nao prejudica o tempo operatorio e que,principalmente,nao compromete a radicalidade, podendo ser considerada em serviços nao especializados e naqueles que eventualmente tratam de pacientes portadores de cancer da regiao cervico-facial.