Autonomic dysreflexia (AD) is not an uncommon clinical condition and it is usually detected in patients with complete spinal injuries at or above thoracic 6th vertebral level (T 6). This condition is reported to occur in 48- 60% of cases of spinal cord injury at or above the level of T6. But AD due to injury below T6 is rare. The basic mechanism is thought to be due to excessive, uncontrolled activation of sympathetic system. In the present case, we discuss a persistent AD in 55-yr-old tetraplegic patient with C5 American Spinal Injury Association (ASIA) grade A lesion due to a fall from 10 metre height. MRI examination showed C5 and C6 bi-facets fracture and dislocation with canal compromise. Wiring and fusion was performed but recurrent mucous plugging and aspiration pneumonia and urinary tract infection happened during the hospital stay. Three months later, he was re-admitted with multiple pressure sores, pneumonia, sepsis and high blood pressure. He was administered with nifedepine but the blood pressure kept fluctuating. The present study highlights how the precipitating factors like concomitant urinary tract infection, decubitus ulcers, spasticity triggered the AD attack. The knowledge of the AD and its proper diagnosis and management may be beneficial to all clinicians and the present article attempts to highlight such.
A 48-year-old male with complete tetraplegia C6 presented with sweating and flushing of the right half of the face and neck that recurred when lying in supine and left lateral positions. The symptoms subsided immediately upon sitting upright or lying in a right lateral position. The symptoms were associated with occasional mild head discomfort rather than headache and were accompanied by marked elevation of blood pressure, which was 190-200/120-130 mmHg compared to his previous baseline blood pressure of 80-90/50-70 mmHg, and he had a heart rate of 60-70 beats per minute. We believe that post-traumatic syringomyelia, found upon further investigation, was the cause of the Autonomic dysreflexia (AD) in this patient. He was advised to avoid the positions causing the symptoms and the progression of symptoms was monitored regularly. AD might not have been diagnosed in this patient because of the atypical and unusual presentations. Therefore, knowledge and a heightened level of awareness of this possible complication are important when treating individuals with spinal cord injury (SCI).
A prospective cohort study was conducted to determine the incidence of progressive encephalopathy (PE) and its associated clinical manifestations amongst a cohort of HIV infected children attending the HIV/AIDS clinic of the Pediatric Institute, Kuala Lumpur Hospital, Malaysia. Neurological and neurobehavioral assessments were performed in 55 children with HIV over a 24-month study period. Parameters assessed were physical and neurological assessments, CD4 counts, CD4 percentages, RNA viral loads and an IQ assessment at four monthly intervals. PE was diagnosed when patient developed at least one of the definitive criteria for PE based on the Consensus of Pediatric Neurology/Psychology Working Group, AIDS Clinical Trial 1996. The incidence of encephalopathy was 18.2% (n = 10) in 2002. All the patients had hepatosplenomegaly, lymphadenopathy, abnormal deep tendon reflexes and five had impairment in brain growth. The CD4 counts and CD4 percentages were more likely to be associated with PE compared to the non-PE group.