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)

We are reporting an autopsy case of so-called "acute multiple sclerosis" that was difficult to differentiate from a brain tumor on MRI findings. This case was a 69-year-old man, whose initial symptoms consisted of headache and unsteadiness in walking. Neurological findings included mild ataxia of the left upper extremity and positive Romberg sign. T 2-weighted MRI showed high intensity areas in the posterior limb of the right internal capsule and white matter near the posterior horn of the right lateral ventricle. Although the headache improved, the unsteadiness was exacerbated and the patient became unable to keep standing. Psychiatric symptoms and left hemiparesis were added to the clinical picture. The following MRI proved expansion of the previous lesions and the diffusely enhanced lesion spreading into the contralateral side through the corpus callosum. Stereotaxic biopsy showed the perivascular accumulation of small lymphocytes and a large number of bizarre astrocytes. Primary brain malignant lymphoma was diagnosed and radiation therapy was carried out. However, he developed perforation of the intestinal tract and died. Autopsy findings revealed scattered and disseminated small lesions in the cerebral white matter and the corpus callosum. There were a large number of lipid-laden macrophages, no stainable myelin and preserved axis cylinders in those lesions. Thus, those were interpreted as demyelinting lesions. They were scattered and multiple. This case was radiologically characterised by the diffusely enhanced, expanding butterfly-shaped lesion in bilateral cerebral hemisphere through the corpus callosum, and pathologically proven to be acute demyelination associated with severe perivascular infiltration of inflammatory cells. Multiple sclerosis may mimic neoplastic processes as trans-callosal hyperplastic neuroimage on neuroimaging like the present case.
 ...
PMID:[A clinico-pathological study of so-called "acute multiple sclerosis" mimicking a brain tumor on the MRI findings]. 1039 Oct 75

The vestibulospinal system was evaluated using a stabilometric method in patients with migraine and episodic tension-type headache during headache-free periods. Migraine patients often complain of dizziness or vertigo during headache attacks and some exhibit these symptoms between attacks. Computerized static stabilometry is a reliable and non-invasive technique to evaluate the equilibrium function in various diseases. The subjects consisted of 21 patients with migraine, 12 patients with episodic tension-type headache and, age- and sex-matched controls. We performed two sets of static stabilometric measurements with eyes open (EO) and eyes closed (EC) for 30 s. The averages of two sessions of the following six stabilometric parameters were used for the analysis: locus length (LNG), environmental area (ENV-AREA), rectangle area (REC-AREA), locus length per second, locus length per environ area (L/E), and root mean square area. Romberg quotients (EC/EO) of these six parameters were also analyzed. The mean values of LNG, ENV-AREA and REC-AREA in the EC session in the migraine group were significantly greater than those in the controls (P < 0.05, Mann-Whitney rank sum test). Romberg quotients of all stabilometric parameters except the L/E in the migraine group were significantly greater than in the controls. Patients with episodic tension-type headache did not show any differences in the stabilometric study from the controls. The present findings suggest that patients with migraine show a significant increase of the body sway during the EC session, which indicates an underlying dysfunction in the vestibulospinal system.
 ...
PMID:Static stabilometry in patients with migraine and tension-type headache during a headache-free period. 1192 75

The aim of this paper is to present a case of acute occupational mercury poisoning treated at the Clinical Department of Occupational Diseases. A welder, forty years old was employed at a large chemical plant in the dissembling department involved in the production of acetaldehyde. The patient was referred to the hospital by an occupational physician. During his shift; dissembling mercury-covered tubes a nausea, abdominal pain and elevated temperature occurred. He was also complaining of headache and symptoms of gingivitis, which lasted two weeks before hospitalization. Before admission to the Clinical Department, mercury concentrations in urine were measured twice. The urine mercury levels were very high, impossible to determine precisely. During hospitalization, the patient was complaining of head and gingiva pains. Since the symptoms persisted and high urine mercury levels (830 micrograms/l) were determined--DMPS--Heyl was administered. After treatment symptoms subsided and the concentration of mercury in urine was gradually returning to normal. The results of laboratory tests did not reveal any impairment of internal organs. Consultant in neurology found the presence of nystagmus and positive Romberg test in the patient. Neurological signs disappeared after a month. The measurements performed by the Department of Work Safety revealed high exceeded hygiene permissible limits of mercury vapors in the air. The information provided by the employer's technical services also showed that the patient was working with the face mask, but its absorber was not readjusted to mercury vapors. A control ambulatory examination (one and a half year later) did not reveal health effects of acute exposure to mercury vapors.
 ...
PMID:[Occupational acute mercury intoxication--a case report]. 1247 11

We report beneficial and adverse effects of sodium dichloroacetate (DCA) in three adult Japanese patients with mitochondrial disease: a 21-year-old male with involuntary movements, optic atrophy, hearing loss, and convulsions (patient 1), a 28-year-old man with mental deterioration, hemianopia, hearing disturbance, and convulsions (patient 2), and a 50-year-old woman with hearing disturbance, generalized muscle atrophy, and insulin dependent diabetes mellitus (patient 3). A3243G mutation was found in patient 2 and patient 3. Oral administration of DCA improved consciousness level and gait disturbances in patient 1, and ameliorated headaches, easy fatiguability, and muscle cramps in patient 2 and patient 3. DCA normalized high levels of lactate and pyruvate in blood and cerebrospinal fluids in all three patients. In patient 3, daily insulin needs decreased from 38 to 24 units, and urine C peptide increased from an undetectable level to 16 micrograms/day. In patient 1, DCA 23 mg/kg/day had been beneficial without adverse effects and he became free of convulsions for more than 32 months. However, despite of normal lactate and pyruvate, unsteady gait and lethargy developed after 50 mg/kg/day treatment for two months and one month in patient 2 and patient 3, respectively. In both patients, deep tendon reflexes disappeared and Romberg sign became positive. Nerve conduction studies confirmed sensory-dominant polyneuropathy and electroencephalogram showed diffuse slow basic activities. Cessation of DCA resulted in recovery of gait and consciousness, but sensory nerve action potentials did not recover in one month. Long term treatment of 50 mg/kg/day DCA may affect adversely the peripheral and central nervous systems in adult patients. Although effective plasma DCA concentration was previously reported as 25-160 micrograms/ml in patients under 18 years old, plasma DCA concentration of 10.2 micrograms/ml was sufficient in patient 1. We recommend lower dose of DCA in adult patients than in child patients.
 ...
PMID:[Dichloroacetate treatment for adult patients with mitochondrial disease]. 1289 50

A 50-year-old African American woman presented with bilateral lower extremity pain, a history of falls during the past several months, and personality and behavior changes. She had been in good health until approximately 5 months before admission, when she began to fall with increasing frequency, often while going down a flight of stairs. She described these falls as her "legs giving out" and feeling very heavy and unsteady. There was no head trauma or loss of consciousness. Her daughter noticed that her gait had become somewhat unsteady during the last several months. Her family also noted a change in her personality at this time. Previously, she had been a very tidy person who took great care with her appearance, who was working as a customer service representative. However, she had become less social and very withdrawn. She had been observed putting on dirty clothes after showering, as well as eating constantly. The patient denied any fevers, chills, night sweats, headaches, vision changes, or tinnitus. She also denied any rashes, muscle pain, or intolerance to heat or cold. There was no history of seizure disorder or depression. Her past medical history was notable only for hypertension and being a passenger in a motor vehicle crash 1 year before admission. She denied any alcohol, tobacco, or illicit drug use, and had no travel history other than coming to the United States, as she was originally from Trinidad. On physical examination, she was a moderately obese African American woman with a flat affect, psychomotor slowing, and alopecia of the scalp. She was alert and oriented to person, place, and time, but had a score of 26 out of 30 on the Mini-Mental State Examination. She lost points only for recall; she had no difficulty with serial 7s. Her cranial nerves were intact and her speech was fluent, although sparse, and she did not make any paraphasic errors. Her muscle strength was 5/5 in both the upper and lower extremities. Reflexes were 2+ in the upper extremities and 1+ in the lower extremities, and toes were downgoing bilaterally. She had intact sensation to light touch and pinprick, but markedly diminished proprioception of her lower extremities bilaterally. She had a wide-based gait with a positive Romberg sign and was markedly ataxic. Rectal examination yielded a positive guaiac test with brown stool, normal tone, and no masses. The remainder of the physical examination was normal. Laboratory studies revealed pancytopenia with a hematocrit of 22.7% and a mean corpuscular volume of 118.2 fL. A peripheral smear that was performed on admission, prior to transfusion, revealed macrocytic red cells and hypersegmented neutrophils.
 ...
PMID:Cases from the Osler Medical Service at Johns Hopkins University. 1465 20

We have observed in our own practice that numerous patients with primary symptoms of vertigo exhibit cervical segmental muscular imbalance and increased tension in the masticatory musculature. This is frequently associated with functional blockades, especially in the joints of the head and upper cervical spine. Particularly important are special receptors of the small vertebral joints and muscle insertions at the cervicocranial transition. Evidence indicates that there are neuroanatomic structures between these receptors and the central vestibular and cochlear core area of the brain stem, which can explain the vertigo symptoms as well as the frequently associated tinnitus, headache or otalgia. Therapeutic approaches include interruption of the pathological reflex arcs so that muscle tension can resolve and imbalances are equalized. The nociceptive stimulus to the brain stem and its core centers thus recedes. Deafferentation follows from the reflex zones of the posterior oral cavity in the sense of oral acupuncture. Additional procedures include neural therapeutic injections at acupuncture points at the cervicocranial transition, the ear, and maxillary area as well as needle acupuncture of the head, ear, and hand. In isolated cases, improvement of the vertigo symptoms is noticed as early as after the first treatment session. Among other methods, spinovestibular tests according to Romberg and Unterberger can be employed to objectify treatment results.
 ...
PMID:[Additive treatment for central vestibular vertigo]. 1545 63

Progressive Hemifacial Atrophy, also known as Parry-Romberg Syndrome, is an uncommon degenerative and poorly understood condition. It is characterized by a slow and progressive atrophy affecting one side of the face. The incidence and the cause of this alteration is unknown. A cerebral disturbance of fat metabolism has been proposed as a primary cause. This can be the result of a trophic malformation of Cervical Sympathetic Nervous System. Possible factors that are involved in the pathogenesis include trauma, viral infections, heredity, endocrine disturbances and auto-immunity, among others. The most common complications that appear in association to this health disorder are: trigeminal neuritis, facial paresthesia, severe headache and epilepsy, being this last one the most frequent complication of the Central Nervous System. Characteristically, the atrophy progresses slowly for several years and, soon after, it become stable. Now, plastic surgery with graft of autogenous fat can be performed, after stabilization of the disease, to correct the deformity. Orthodontic treatment can help in the correction of any associated malformation. The objective of this work is, through the presentation of a clinical case, to accomplish a literature review concerning general characteristics, etiology, physiopathology, differential diagnosis and treatment of progressive hemifacial atrophy.
 ...
PMID:Progressive Hemifacial Atrophy--case report. 1650 85

We report a case of Parry-Romberg syndrome in a 32-year-old woman presenting with intermittent headache and mild sensory disturbance. MR imaging revealed minimal asymmetric atrophy of the right hemisphere with a few nonspecific white matter hyperintensities. Diffusion tensor imaging and fiber tractography, however, demonstrated clear fiber derangement, especially in the sensory tract of the right cerebral white matter.
 ...
PMID:Diffusion tensor imaging and fiber tractography in Parry-Romberg syndrome. 1820 29

We present a 30-year-old South Indian man who presented with complaints of left sided headache and facial pain for past 3 months, severe for past 10 days. On physical examination, right side of the face appeared normal. Left side of the face showed signs of hemi atrophy with minimal drooping of left eyelid. All Systems were found to be normal. Routine blood and urine investigations results were within normal limits. X-ray chest revealed no abnormalities and x-ray skull showed both sides equal. Computerized tomogram of the brain showed left minimal sub dural hygroma with no midline shift, and no evidence of cerebral edema or cerebral atrophy. Nerve conduction study showed features suggestive of trigeminal neuralgia. MRI of the skull base was also normal and showed no evidence of trigeminal nerve compression. Interestingly, he had minimal response to analgesics, steroids, and propranolol, but showed immediate response to carbamazepine. Hence this patient indeed had Parry Romberg syndrome: Hemi facial atrophy with trigeminal neuralgia.
 ...
PMID:Progressive hemi facial atrophy - Parry Romberg syndrome presenting as severe facial pain in a young man: a case report. 1982 58

A 29-year-old man, with no significant past medical history, was in his usual state of health until the afternoon of admission. The patient was seated at work eating lunch when he suddenly noticed that his vision became blurry. He covered his right eye and had no visual difficulty but noted blurry vision upon covering his left eye. At this point, the patient tried to stand up, but had difficulty walking and noticed he was "falling toward his left." Facial asymmetry when smiling was also appreciated. The patient denied any alteration in mental status, confusion, antecedent or current headaches, aura, chest pains, or shortness of breath. He was not taking any prescribed medications and had no known allergies. The patient denied any prior hospitalization or surgery. He denied use of tobacco, alcohol, or illicit drugs, and worked as a maintenance worker in a hotel. His family history is remarkable for his father who died of pancreatic cancer in his 50s and his mother who died of an unknown heart condition in her late 40s. Vital signs on presentation to the emergency department included temperature of 97.6 degrees F; respiratory rate of 18 per minute; pulse of 68 per minute; blood pressure of 124/84 mmHg; pulse oximetry of 99% on ambient air. His body mass index was 24 and he was complaining of no pain. The patient had no carotid bruits and no significant jugular venous distention. Cardiovascular exam revealed a regular rate and rhythm with no murmurs. Neurological exam revealed left-sided facial weakness, dysarthria, and preserved visual fields. He was able to furrow his brow. Gait deviation to the left was present, and Romberg sign was negative. Deep tendon reflexes were 2+ throughout, and no other focal neurological deficit was present. The patient was admitted to the hospital with a diagnosis of stroke. Electrocardiogram, fasting lipid profile, computed tomography (CT) scan of head, magnetic resonance imaging (MRI) of head and neck, and transthoracic echo with bubble study were ordered. The initial head CT did not reveal bleeding. He was started on aspirin (ASA). On the second hospital day, the symptoms improved with resolution of dysarthria. His ataxia had also improved. Fasting lipid profile revealed mildly elevated low-density lipoprotein and total cholesterol. His head MRI revealed an acute right thalamic stroke. Echocardiography was significant only for a patent foramen ovale (PFO) with transit of agitated saline "bubbles" from right atrium to left heart within three cardiac cycles (Figure). Doppler ultrasound of extremities revealed no evidence of deep venous thrombosis. A complete resolution of symptoms occurred by the third hospital day. The patient was discharged on full dose aspirin and a statin and was referred for consideration of enrollment in a PFO closure versus medical management trial.
 ...
PMID:Clinical case of the month. A 29-year-old man with acute onset blurry vision, weakness, and gait abnormality. Stroke. 2010 23


<< Previous 1 2 3 4 5 Next >>