Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies]. 766 22

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85

Patients suffering from vascular disease are often a challenge for the acute pain service. Ischaemia, impaired wound healing, stump and phantom limb pain often require a complex analgesic regimen. Invasive measures such as spinal or epidural catheters can be very helpful but carry the risk of infection, as shown by this case report. A 53-year-old woman with a ten-year history of diabetes developed arterial vascular disease. Her right lower leg had been amputated two years previously. She was now admitted with necroses of the left forefoot. A bypass operation was performed under general anaesthesia. Because of intractable ischaemic pain, she was provided with an epidural catheter by the acute pain service. The bypass occluded, however, and a few days later her left lower leg also had to be amputated, this operation being performed under epidural anaesthesia with bupivacaine. The catheter was subsequently used for postoperative pain control and as a means to prevent phantom limb pain. When signs of superficial catheter infection were noticed days later, the catheter was immediately removed. Intractable pain then developed in the left leg which could not be sufficiently controlled with opioids and NSAIDs, and so a second epidural catheter was inserted one segment rostrally. Several days later the infected vascular prosthesis had to be removed followed by amputation of the thigh, this operation also being performed in epidural anaesthesia. Eleven days after insertion of the first epidural catheter, the patient complained of low back pain and headache. Examination by a neurologist revealed no signs of intraspinal infection. The second epidural catheter dislocated at this point in time and it was decided to introduce a third one, this being the only means to treat the otherwise intractable stump pain. Ten days later meningism, Kernig's sign and leucocytosis developed. NMR tomography detected intraspinal fluid in the epidural space at the dorsal border of the spinal canal. A hemilaminectomy was performed. The spinal epidural space showed signs of inflammation of the adipose tissue, but no pus. A little necrotic material and residues of an old haematoma were removed and the epidural space was lavaged. Specimens taken from the epidural material revealed colonisation with staphylococcus epidermidis, which was sensitive to the broad spectrum antibiotics formerly given to the patient to treat the infection in the left stump. By the next day, all signs of epiduritis had disappeared and the patient recovered completely.
 ...
PMID:[Epiduritis after long-term pain therapy with an epidural catheter--review of the literature with a current case report]. 932 67

We report here the clinical presentation and subsequent autopsy of a 90-year-old man who developed small papules with pain and swelling in his right ear. On admission, he exhibited right facial nerve paralysis, neck stiffness and Kernig's sign. The cell count was elevated and the varicella-zoster virus-PCR was positive in the CSF. Brain magnetic resonance imaging showed hyperintense lesions in the left pons and left temporal lobe, in FLAIR images. We diagnosed the patient with Ramsay Hunt syndrome and meningoencephalitis due to varicella-zoster virus. Although the symptoms of meningitis improved following treatment with intravenous acyclovir (750 mg/day initially, raised to 1,125 mg/day), 16 days after admission, he died suddenly due to gastrointestinal hemorrhage. The autopsy findings included lymphocytic infiltration of the leptomeninges and perivascular space of the cerebrum, and slight parenchyma in the left temporal lobe and insula, as the main histological features. Encephalitis due to varicella zoster virus has been recognized as a vasculopathy affecting large and small vessels. Pathological confirmation is rare in varicella zoster virus meningoencephalitis.
 ...
PMID:[An Autopsy Case of Meningoencephalitis and Cerebral Infarction that Developed with Ramsay Hunt Syndrome and Disseminated Herpes Zoster]. 2951 69