Fabio Formaglio

The Lindblom roller

Neuropathic pain is caused by injury of the peripheral or central nervous system. The neurological examination of the sensory system in neuropathic pain patients guides the anatomical localization of the injury. Among the sensory modalities to be tested, priority should be given to those subserved by small peripheral sensory fibers or by the spinothalamic tract that most commonly are abnormal in neuropathic pain patients. Testing of cold and warm perception was traditionally carried out in the clinic using tubes filled with water at different temperatures, a cumbersome method that has limited the routine examination of these sensory modalities. The Lindblom roller offers a practical and effective method of readily testing temperature perception and is among the best available clinical tools for delineating the anatomical boundaries of a sensory abnormality. Routinely use of the Lindblom roller shall be standard bedside clinical assessment of neuropathic pain patients. To exemplify this statement we describe two patients affected by complex and fluctuating painful sensory abnormalities caused by an extradural mass compressing the spinal cord. The level of the injury was readily localized with a roller kept at room temperature.

Central effect of Ketorolac involving NMDA receptors activity

Possible central mechanisms underlying the analgesic action of Ketorolac, a non-steroidal antiinflammatory drug (NSAID) have been investigated using an iontophoretic approach. We found that the excitation induced by N-methyl-d-aspartate (NMDA) on spinal wide dynamic range (WDR) neurons was prevented, or reduced, by Ketorolac applied before or after the start of the NMDA ejection. The data suggest that Ketorolac can achieve its central analgesic effect by interfering with the NMDA receptor activity on the spinal neurons.

Sensory disorder of the chest as presenting symptom of lung cancer.

Four patients with pancoasts syndrome had burning pain in the axilla and abnormal sensation in the intercostobrachial nerve territory. The intercostobrachial nerve is the first component of the brachial plexus to be invaded by lung tumours.

Acute myelopathy selectively involving lumbar anterior horns following intranasal insufflation of ecstasy and heroin

We report a patient who developed acute myelopathy after intranasal insufflation of amphetamines and heroin. The functional prognosis was very poor; after 4 months, she remained paraplegic. MRI imaging showed selective T2 hyperintensity and intense enhancement confined to the spinal anterior horns and lumbar nerve roots and plexus. This unique MRI pattern, together with neurophysiological data, suggests that the pathological process at the first primary affected spinal anterior horns (SAH), conditioning motoneuron cell death, and then nerve roots and lumbar plexus as a consequence of wallerian degeneration A 17-year-old girl was admitted to the emergency department in a drowsy state and unable to walk after an overdose of intranasal insufflated heroin and amphetamines. After a few hours, drowsiness progressed to stupor, and progressive weakness in all four limbs, mainly involving the lower limbs, developed. At that time, laboratory data showed massive rhabdomyolysis (creatine phosphokinase 36 880 mg/dl) with acute renal failure (ARF), and hepatic failure; medical therapy was promptly started. The patient’s past medical history was unremarkable except for habitual use of amphetamines (ecstasy) and cannabinoids since the age of 12 years. The previous week she had insufflated heroin about once a day; the previous night she reported a double dose of heroin consumption, and a high dose (approximately 1 g) of intranasal insufflation of amphetamines. The next day the …

Acute myelopathy selectively involving lumbar anterior horns following intranasal insufflation of ecstasy and heroin.

We report a patient who developed acute myelopathy after intranasal insufflation of amphetamines and heroin. The functional prognosis was very poor; after 4 months, she remained paraplegic. MRI imaging showed selective T2 hyperintensity and intense enhancement confined to the spinal anterior horns and lumbar nerve roots and plexus. This unique MRI pattern, together with neurophysiological data, suggests that the pathological process at the first primary affected spinal anterior horns (SAH), conditioning motoneuron cell death, and then nerve roots and lumbar plexus as a consequence of wallerian degeneration