He Cried While Clutching His Arm — What Is 'Eating' His Nerves Slowly?

He Cried While Clutching His Arm — What Is 'Eating' His Nerves Slowly?. In a small village in Kelantan, a high school teacher suddenly could not lift a textbook—not because of weakness, but because his nerves were being 'eroded' from within. This is not a stroke. Not a tumor. Not even ordinary fatigue. It is Hereditary Neuralgic Amyotrophy: a rare and painful condition that feels like repeated lightning strikes in the nerves, and can be inherited without anyone knowing.. The First Voice That Was Never Forgotten The voice was not a scream. Not a whimper. It was softer—like the hiss of air trapped under the skin, followed by an odd tremor in the left shoulder. Dr. Aminah recalls hearing this sound for the first time from a 32-year-old patient at the neurology clinic of Universiti Sains Malaysia Hospital. It was not an ordinary sound. It was the sound of a nerve breaking . The patient—a fisherman from Pulau Langkawi—described the feeling as 'thousands of hot needles being inserted into the shoulder joint and then slowly pulled out.' In medical records, it is documented as 'proximal acute neuralgia,' but in human terms: this is the beginning of loss—not just muscle strength, but trust in one's own body. An Invisible Inheritance in DNA Hereditary Neuralgic Amyotrophy HNA is not a disease that comes from outside. It is born from within—from a mutation in the SEPT9 gene on chromosome 17q25, a minor error in the code of life that makes up less than 0.0001% of the entire human genome. Yet, this tiny mistake is enough to disrupt the structure of septin—a protein that acts like a 'microscopic scaffold' in nerve cells. When septin fails to function, the brachial and cervical fascia nerves become fragile. They can no longer transmit signals smoothly. And when physical stress or a mild infection appears—such as a common cold or even a routine vaccination—the immune system mistakenly attacks the nerves themselves. It is not full autoimmunity, but more like a 'misidentification' in the body's defense team. Approximately 50% of HNA cases are linked to this mutation. The rest? Still a mystery—like rain falling without clouds. Unwarned Attacks: Between Pain and Loss Each HNA attack happens like a storm with no weather forecast. It starts with severe pain—not ordinary pain, but pain that erases the boundary between 'me' and 'my body.' Patients often report losing sensation before losing function: fingers suddenly go numb, then they cannot grip, then they cannot lift their arms above their heads. Within 48 hours, muscle atrophy becomes visible—not because the muscles are unused, but because the nerves no longer send instructions. The muscles 'forget' how to contract. At the neurology clinic in Kota Bharu, a 17-year-old boy—son of a teacher who had previously suffered similar attacks—shows his right arm, which is now 3 cm smaller than the left. It is not a congenital deformity. It is a biological history rewritten by genes. The Shadow of Parsonage-Turner: One Syndrome, Two Faces HNA is often mistaken for Parsonage-Turner Syndrome PTS , as its clinical symptoms are almost identical: acute neuralgia, proximal muscle weakness, and progressive atrophy. But the difference is not on the surface—it is hidden in the family lineage. PTS is usually sporadic, appearing once in a lifetime, and is not inherited. HNA, however, can recur repeatedly—sometimes every two to five years—and each attack can leave deeper disabilities. A patient in Sabah experienced four attacks over 12 years. Each time, he lost more shoulder and arm function. However, the long-term prognosis is unique: although recovery is not complete, most patients do not experience systemic disabilities or life-threatening conditions. The brain, heart, and lungs remain intact. Only the peripheral nerves—those that enable movement, grasping, and touching the world—are 'injured.' Between Diagnosis and Silence Diagnosing HNA remains a challenge. There is no specific blood test. No clear MRI images showing lesions. It is built from stories: from family histories, from attack patterns, from exclusions. Electromyography EMG may show reduced nerve activity, but it is often normal in the early stages. SEPT9 gene sequencing is the only definitive confirmation—but it is not available in most health centers in this region. As a result, many patients are misdiagnosed for months, even years, as 'emotional stress,' 'chronic fatigue,' or 'orthopedic problems.' At a private clinic in Johor Bahru, a 41-year-old woman underwent seven orthopedic examinations before finally being referred to a neurogenetic specialist—and only on her 11th visit did the name 'Hereditary Neuralgic Amyotrophy' appear clearly. It is not just a diagnosis. It is an acknowledgment: that her pain is real, her inheritance is valid, and her loss is not a fantasy. What Remains: Voice, Memory, and the Right to Know What is most touching is not the loss of muscle—but the loss of narrative. Many HNA patients have never read the name of their disease in their native language. There are no brochures in Malay. No local support communities. No documentaries. No songs. They live with a 'nameless disease'—until today. But in every attack, something remains: their voices that can still tell stories, their fingers that can still write their children's names on paper, and their eyes that can still gaze into the eyes of those they love—without needing to raise their arms. Hereditary Neuralgic Amyotrophy may eat nerves, but it never eats the soul. And in the darkness of information absence, the first light is the correct name—because a name is the beginning of everything: recognition, healing, and hope that is not inherited, but chosen. Rujukan: Hereditary neuralgic amyotrophy — Wikipedia https://en.wikipedia.org/wiki/Hereditary neuralgic amyotrophy