Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the publication by F. Vourc'h in 1963 [Br J Anaesth (1963) 35:118-120] describing the use of a plastic catheter inserted percutaneously for the drainage of lumbar cerebrospinal fluid (CSF) the indications for spinal drainage are numerous, but not very well systematized. The bibliographical review shows few recent papers concerning the techniques, indications, complications and pitfalls. The authors considered it interesting to analyze nine papers, in particular those dedicated to the use of spinal drainage in skull base surgery and in the prevention and/or treatment of CSF fistulas. Two papers describe for the first time pachymeningeal gadolinium enhancement associated with orthostatic headaches, owing to CSF hypotension mimicking an inflammatory or infiltrative disease. The results of the treatment of CSF fistulas are good with a high success rate, avoiding direct surgical repair. The use of a specially designed subarachnoid catheter is clearly superior to the epidural catheter, with good flow of CSF and minimal complications. The main problems are deficient flow and infections. Overdrainage is potentially dangerous, with acute pneumocephalus, brain collapse and neurological deterioration. Infrequent but possible is Chiari II-like syndrome with vocal cord paralysis and life-threatening aspiration, or temporal downward herniation with kinking of the posterior cerebral artery and acute brain infarct. The key to success lies in a rigid protocol, intermittent CSF drainage with a closed circuit, and daily biochemical and microbiological monitoring. Highly qualified medical and nursing staff are essential.
 ...
PMID:Cerebrospinal fluid spinal lumbar drainage: indications, technical tips, and pitfalls. 993 64

A 45-year-old woman had pyrexia, headaches, collapse and hyponatraemia. Intracerebral abscess, bacterial meningitis and subarachnoid haemorrhage were excluded. She was given intravenous antibiotics and gradually recovered. One month later she was readmitted with diplopia, headache and vomiting. Serum sodium was low (107 mmol/l) and a diagnosis of inappropriate ADH secretion was made. MRI scan showed a suprasellar tumour arising from the posterior pituitary gland. A skin rash gradually faded. Serum cortisol, prolactin, gonadotrophins and thyroid hormone levels were low. A pituitary tumour was removed trans-sphenoidally, she had external pituitary radiotherapy, and replacement hydrocortisone and thyroxine. She was well for 12 months when she developed progressive weakness and numbness of both legs. Examination suggested spinal cord compression at the level of T2 where MRI scanning showed an intradural enhancing mass. This spinal tumour was removed and her neurological symptoms disappeared. Nine months after this she developed facial pain and nasal obstruction. CT scan showed tumour growth into the sphenoid sinus and nasal cavities. A right Cauldwell-Luc operation was done and residual tumour in the nasal passages was treated by fractionated external radiotherapy and Prednisolone. Histological examination of the specimens from pituitary, spinal mass, and nasal sinuses showed Rosai-Dorfman disease, a rare entity characterized by histiocytic proliferation, emperipolesis (lymphophagocytosis) and lymphadenopathy. Aged 48 she developed cranial diabetes insipidus. Although Rosai-Dorfman syndrome is rare, it is being reported with increasing frequency, and should be borne in mind as a possible cause of a pituitary tumour.
 ...
PMID:Rosai-Dorfman disease presenting as a pituitary tumour. 1034 67

A 40-year-old man presented with intractable headache of 5-year duration and a 1-month history of intermittent cerebrospinal fluid (CSF) rhinorrhea. Magnetic resonance imaging showed a cystic lesion with signal characteristics similar to that of CSF. The patient underwent endonasal endoscopic surgery of the sphenoid sinus and the fistula was reinforced with facia, muscle cartilage, and posterior septal flap while performing cystocisternostomy. The postoperative course was uneventfiul CSF leakage stopped, and headache improved. Postoperative imaging revealed total collapse of the cyst cavity. Based on our findings, endonasal endoscopic treatment of the sellar and parasellar arachnoid cysts, if presenting into the sphenoid sinus, could be an acceptable minimally invasive alternative to the conventional modalities.
 ...
PMID:Endonasal endoscopic treatment of parasellar arachnoid cyst: report of a case. 1189 95

We report a case of fatal intoxication with 2% viscous lidocaine. A 18 month old infant was admitted after malaise and cardiorespiratory arrest at home. He was resuscitated, then seizures appeared before arrival at the hospital. Treatment was symptomatic, including cardiorespiratory resuscitation and administration of anticonvulsants. Identification of lidocaine and its metabolite monoethylglycinexylidide (MEGX) MEGX was performed after organic extraction by High Performance Liquid Chromatography (HPLC) with Diode Array Detection (DAD); the serum concentrations, determined by Fluorescence Polarisation Immuno Assay (FPIA), were: 1.1 micrograms/ml for lidocaine and 0.94 microgram/ml for MEGX (H + 7) and 0.30 microgram/ml for the lidocaine (Day + 1). Neurotoxic manifestations appear at lower concentrations than cardiotoxic symptoms which are correlated with plasma levels of lidocaine. The toxic symptoms begin with headache, hallucinations, seizure, coma, respiratory arrest and circulatory collapse. The toxic symptoms can persist even after the decrease of lidocaine concentration under therapeutic levels. There is no antidote and acute lidocaine toxicity is managed with supportive therapy (diazepam for seizures, intubation, chronotropic agents). Considering the gravity of these poisonings which remain rare, the 2% viscous lidocaine prescription is forbidden for children under 6 years old.
 ...
PMID:[Fatal intoxication after accidental ingestion of viscous 2% lidocaine in a young child]. 1197 45

Microbiological, biological, and chemical toxins have been employed in warfare and in terrorist attacks. In this era, it is imperative that health care providers are familiar with illnesses caused by these agents. Botulinum toxin produces a descending flaccid paralysis. Staphylococcal enterotoxin B produces a syndrome of fever, nausea, and diarrhea and may produce a pulmonary syndrome if aerosolized. Clostridium perfringens epsilon-toxin could possibly be aerosolized to produce acute pulmonary edema. Ricin intoxication can manifest as gastrointestinal hemorrhage after ingestion, severe muscle necrosis after intramuscular injection, and acute pulmonary disease after inhalation. Nerve agents inhibit acetylcholinesterase and thus produce symptoms of increased cholinergic activity. Ammonia, chlorine, vinyl chloride, phosgene, sulfur dioxide, and nitrogen dioxide, tear gas, and zinc chloride primarily injure the upper respiratory tract and the lungs. Sulfur mustard (and nitrogen mustard) are vesicant and alkylating agents. Cyanide poisoning ranges from sudden-onset headache and drowsiness to severe hypoxemia, cardiovascular collapse, and death. Health care providers should be familiar with the medical consequences of toxin exposure, and understand the pathophysiology and management of resulting illness.
 ...
PMID:Microbiological, biological, and chemical weapons of warfare and terrorism. 1207 87

Risperidone is an atypical antipsychotic used in the treatment of several psychiatric disorders in both children and adults. We present two patients with hydrocephalus and learning difficulties who were admitted to the neurosurgical unit with a suspected cerebrospinal fluid shunt malfunction and raised intracranial pressure. They had both been commenced on risperidone for the treatment of aggressive outbursts. Twelve days after commencing risperidone, the first patient developed symptoms of headache, nausea, vomiting, drowsiness, lethargy and two episodes of collapse. The second patient presented with similar symptoms 4 days after his risperidone dose was increased. An unnecessary shunt exploration was averted in both cases when it was noted that the side-effect profile of risperidone mimicked exactly those of shunt malfunction. Discontinuation of the drug resulted in complete resolution of all symptoms within 72 h. Many patients with shunted hydrocephalus have associated developmental disorders that may warrant treatment with risperidone. Clinicians should be aware of the potential symptom overlap between shunt malfunction and risperidone side-effects in these patients.
 ...
PMID:Side-effects of risperidone therapy mimicking cerebrospinal fluid shunt malfunction: implications for clinical monitoring and management. 1209 77

Multiple myeloma (MM) is a plasma cell malignancy characterized by infiltration of bone marrow, bone destruction, infiltration of soft tissues with plasma cells, and suppression of normal hematopoiesis. The production of monoclonal immunoglobulins with or without light chains is a major feature of the disease. Full spectrum of plasma cell dyscrasias include monoclonal gammapathy of undetermined significance, smouldering myeloma, indolent multiple myeloma, and fully developed, symptomatic multiple myeloma. The usual presenting features of MM include bone pain, weakness, fatigue, fever and infection. Neurologic symptoms are less common but one must not forget that MM may present with a neurologic disease. Careful neurologic history and examination are mandatory in patients with MM. Neurologic symptoms may be a direct manifestation of MM or may be due to the immune effect of monoclonal proteins directed against different neural structures. Finally, metabolic consequences (uremia, hypercalcemia, hyperviscosity) of MM may produce a broad spectrum of different neurologic symptoms including headache, blurring of vision, drowsiness, precoma, coma, vertigo, ataxia, hemiparesis and epileptiform seizures. The most common location of bone changes in MM is the thoracic spine, where it causes osteolytic changes with consequent compressive fractures. The most disastrous sequel is paraplegia. Multiple vertebral involvement with the evidence of osteolytic changes in other bones is usual, but solitary vertebral myeloma may occur. Myeloma usually involves the bone of the vertebral body and then spreads into the extradural space. However, patients with solitary extradural myeloma have been reported. Skull myeloma is frequently asymptomatic. It may grow externally or, rarely, there is intracranial expansion. Involvement of the cranial nerves is not rare, with II, V, VI, VII and VIII cranial nerves being most often affected. Isolated intracerebral plasmacytomas are extremely rare. Diagnostic approach includes plain X-rays of the skeleton, which was found to be the method of choice for demonstration of osteolytic changes, whereas magnetic resonance with gadolinium enhancement most reliably displays the degree of vertebral involvement and demonstrates any associated soft tissue mass. Current treatment of osteolytic changes in multiple myeloma include chemotherapy, radiotherapy in combination with dexamethasone, monthly infusions of bisphosphonates, surgical decompression, and kyphoplasty. Therapeutic approach is dictated by the presenting symptoms. In case of pain as the predominant symptom, treatment with chemotherapy and radiotherapy may be appropriate. Compressive symptoms are relieved with dexamethasone followed by radiotherapy and chemotherapy. Surgical decompression is used in patients with vertebral collapse and vertebral instability. Kyphoplasty is a new method used in the treatment of osteolytic changes of vertebral bodies. A viscous cement is injected into the cavity by a balloon-like inflatable bone tampon. It has been successfully employed to improve the quality of life, to reduce pain, and to increase overall functioning in patients with vertebral compression fractures by restoring most of the original height of the vertebral body. Bisphosphonates reduce pain associated with osteolytic changes in multiple myeloma, but also significantly reduce skeletal events (pathologic fracture, spinal cord compression, surgery or irradiation of bone) via unknown mechanism. It seems that bisphosphonates, by inhibiting bone resorption, alter the microenvironment in which the MM cells grow.
 ...
PMID:[Neurologic sequelae of bone changes in multiple myeloma and its therapy]. 1263 Mar 41

Carbon monoxide (CO) is a colorless, tasteless, odorless, and non-irritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb), the body's oxygen carrier, forming carboxyhemoglobin (COHb) and thereby reducing oxygen (O(2)) delivery to the body's organs and tissues. High COHb concentrations are poisonous. Central nervous system (CNS) effects in individuals suffering acute CO poisoning cover a wide range, depending on severity of exposure: headache, dizziness, weakness, nausea, vomiting, disorientation, confusion, collapse, and coma. At lower concentrations, CNS effects include reduction in visual perception, manual dexterity, learning, driving performance, and attention level. Earlier work is frequently cited to justify the statement that CO exposure sufficient to produce COHb levels of ca. 5% would be sufficient to produce visual sensitivity reduction and various neurobehavioral performance deficits. In a recent literature re-evaluation, however, the best estimate was that [COHb] would have to rise to 15-20% before a 10% reduction in any behavioral or visual measurement could be observed. This conclusion was based on (1) critical review of the literature on behavioral and sensory effects, (2) review and interpretation of the physiological effects of COHb on the CNS, (3) extrapolation from the effects of hypoxic hypoxia to the effects of CO hypoxia, and (4) extrapolation from rat behavioral effects of CO to humans. Also covered in this review article are effects of chronic CO exposure, the discovery of neuroglobin, a summary of the relatively new role for endogenous CO in neurotransmission and vascular homeostasis, groups which might be especially sensitive to CO, and recommendations on further research. The interested reader is directed to other published reviews of the literature on CO and historically seminal references that form our understanding of this ubiquitous gas.
 ...
PMID:Carbon monoxide and the nervous system. 1266 97

When a disease process becomes life-threatening, it is termed to be malignant. Hyperthermia is a heat illness that arises from one of two basic causes: 1) the body's normal thermoregulatory mechanisms are overwhelmed by the environment (an exogenous heat load) or, more commonly, by excessive exercise in a moderate-to-extreme environment (an endogenous heat load); or 2) failure of the thermoregulatory mechanisms, such as those encountered in the elderly or debilitated patient. Either cause can lead to heat illnesses such as heat cramps, heat exhaustion or heatstroke. Heat cramps are brief, intermittent and often severe muscular cramps that frequently occur in muscles fatigued by heavy work or exercise. They are believed to be caused by a rapid change in the extracellular fluid osmolarity resulting from sodium and water loss. Heat exhaustion is a more severe form of heat illness characterized by minor changes in mental status (poor judgment, irritability), dizziness, nausea and headache. In severe cases, the patient may have an altered LOC. Just as with heat cramps, profuse sweating is present. Removing the patient from the hot environment and administering fluids will usually result in a rapid recovery. [table: see text] Left untreated, heat exhaustion may progress to heatstroke. Heatstroke results when there is a complete collapse of thermoregulatory mechanisms. This will lead to a rise in body core temperature in excess of 105.8 degrees F (41 degrees C), which will produce multisystem tissue damage and physiological collapse. Severe cases can cause death. The patient in this case had an axillary temperature taken and recorded at 101.4 degrees F. Typically, axillary temperatures are one degree cooler than oral temperatures, which are one degree cooler than core temperatures. This patient, then, had a core temperature of 103 degrees F or higher. There are two types of heatstroke: classic and exertional. Classic heatstroke occurs during periods of sustained high ambient temperatures and humidity. Exertional heatstroke more often occurs in athletes, military personnel and people who work strenuosly in the environment. In these situations, endogenous heat accumulates more rapidly than the body can dissipate it in the environment. Although sweating is usually absent in the classic form of heatstroke, 50% of exertional heatstroke cases have persistent sweating as a result of catecholamine release. The presence of sweating does not preclude the diagnosis of heatstroke, and cessation of sweating is not the cause of it. As the illness progresses, peripheral vasodilation occurs, resulting in hypotension and shunting. As internal temperatures rise, myocardial contractility begins to decrease, manifested by bradycardia and irritability of the myocardium. No matter the age group, the presence of hypotension and decreased cardiac output indicates a poor prognosis for the patient.
 ...
PMID:Hot on the inside. 1288 21

Tranylcypromine, a useful antidepressant agent, has been linked with a clinical syndrome of undetermined incidence characterized by exceedingly severe and prolonged headache. Associated phenomena may include paroxysmal hypertension, pallor, chest pain and collapse. This violent reaction does not seem to be related to age, sex, duration of treatment, or pre-existing cardiovascular disease; nor is it possible to predict in whom it will occur. The clinical picture may sometimes be quite similar to that produced by subarachnoid hemorrhage or by pheochromocytoma. The mechanism of action is not known, although it is possible that the syndrome may be due to an amphetamine-like effect; i.e., that tranylcypromine influences the adrenergic component of the reticular activating system. The occurrence of severe headache in the course of tranylcypromine therapy is an indication for immediate withdrawal of the drug. Tranylcypromine cephalgia should be considered as part of the differential diagnosis of sudden, violent and prostrating headache.
 ...
PMID:TRANYLCYPROMINE CEPHALGIA. 1407 36


<< Previous 1 2 3 4 5 6 7 8 9 Next >>