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From Left Beth Smith, Allan Basbaum, Michael Pasternak

To find a cure for excruciating facial pains linked to nerve injury

January 17, 2011 Discussion in San Francisco

From Left Michael Pastenak, Allan Basbaum, Myron Hirsch

 

Nationally known neurobiologist Allan Basbaum, Ph.D., at the University of California San Francisco is focusing on one known cause: the loss of chemical mediators that normally inhibit the transmission of pain signals to the brain. Basbaum is evaluating a unique approach, involving nerve cell transplants, which ultimately may be helpful in treating the persistent electrical shock-like facial pain of trigeminal neuralgia and similar nerve-related facial pain disorders.He explains, “These neuropathic facial pain conditions are often treated with medications designed to suppress the hyperactivity that occurs. Many of these drugs mimic the inhibitory neurotransmitters that normally keep nerves calm. The problem is that although these drugs provide symptomatic relief, they also affect the entire brain and can cause unpleasant side effects from drowsiness to memory loss.”

Basbaum and his colleagues are initiating preclinical studies in genetically altered mice in which they plan to transplant nerve cells that normally secrete the inhibitory chemicals into the trigeminal area of hyperactivity, a treatment expected to restore normal controls over the long term.“Our goal is not only to introduce these healthy nerve cells into the areas of the brain influenced by nerve damage, but to have them fully accepted as an integral part of normal nerve circuitry and to function as intended to normalize the inhibition of pain signals traveling to the brain,” said Basbaum, who chairs the UCSF Department of Anatomy and is editor-in-chief of the journal PAIN.

“The experience of pain typically starts in pain-responsive nerve fibers (nociceptors) that transmit information through axon fibers to nerve circuits in the brainstem, and from there to the brain,” he explains. “But after nerve damage, the pain messages are either misdirected or exaggerated, leading to these neuropathic pains.” “In certain respects, neuropathic facial pain is comparable to what happens in epilepsy,” he said. “Medical scientists for many years have detected an epilepsy-like activity after nerve injury. This is manifest as over-active firing of electrical signals in the brainstem of some patients with trigeminal neuralgia and related chronic facial pain disorders resulting from nerve damage. This is the rationale behind the widespread use of conventional anti-seizure drugs (i.e. Tegretol and Dilantin) to calm the electrical circuitry in the nerves in an effort to reduce pain.”

Because of the hyperactive electrical signals, TN patients often experience a highly exaggerated response to such slight stimuli as a cool breeze across the face, or by chewing, talking, brushing the teeth or combing the hair. Everyday actions that normally evoke no pain at all may trigger excruciating pain, which has been compared to electrical shocks or lightning striking the face. In some individuals, the attacks of facial pain occur spontaneously simply because the pain-inhibiting circuitry in the brainstem is dysfunctional after nerve damage.

Basbaum, who has devoted his entire career to pain research, aims to find a way to restore that circuitry. His UCSF team includes scientists who have genetically engineered mice so that it is possible to monitor the integration of the transplanted cells, as well as developmental neurobiologists who study how inhibitory neurons grow after transplantation and how to make them thrive.  

 

 
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