Biomedical subjects

F Pérez-Errazquin

Publications and source records attributed to F Pérez-Errazquin.

3 recordsLinked to original sources

PubMed1997

[Subacute combined degeneration of the spinal cord: manifestations of esophageal epidermoid carcinoma].

INTRODUCTION: Subacute combined degeneration of the spinal cord associated with vitamin B12 deficit is well known. However a paraneoplastic induced cyanocobalamin malabsorption responsible for either subacute combined degeneration of the spinal cord, has not been reported. Moreover, the possibility of either subacute combined degeneration of the spinal cord may be manifestation of a cancer, it's unknown. CLINICAL CASE: We present the case of a 73-year-old woman with cutaneous paleness and clinical manifestations of a subacute combined degeneration of the spinal cord. Laboratory analysis showed a megaloblastic anemia and Schilling test showed cyanocobalamin malabsorption corrected by intrinsic factor. Anti-intrinsic factor antibodies were positive. Chronic atrophic gastritis and immunological diseases associated with pernicious anemia or with anti-intrinsic factor positive, were excluded. A hidden esophageal squamous cell carcinoma was discovered. Necropsy confirmed both, subacute combined degeneration of the spinal cord and esophageal carcinoma in the absence of chronic atrophic gastritis. CONCLUSIONS: Anti-intrinsic factor antibodies were the only found factor which could explain cyanocobalamin malabsorption. A esophageal squamous cel carcinoma was discovered. In our case, vitamin B12 malabsorption had a paraneoplastic origin mediated by anti-intrinsic factor antibodies. Subacute combined degeneration of the spinal cord may be the manifestation of a hidden esophageal squamous cell carcinoma.

Aged↗

PubMedDate not supplied

[Spontaneous intracranial hypotension].

INTRODUCTION AND CLINICAL CASE: A 38 year old woman, with no previous history of trauma, presented complaining of interscapular pain followed by pulsating headache clearly related to posture, alleviated on lying down and worse on standing up. Subsequently, she also complained of diplopia. On examination there was paresia of the left sixth cranial nerve. Low opening pressure on lumbar puncture confirmed the presence of intracranial hypotension. The protein level of the cerebrospinal fluid was slightly raised. On CT the cortical sulci and small ventricles had disappeared. Cerebral MR (without gadolinium) showed marked diffuse meningeal hyper-intensity and apparent absence of the basal cisterni. Isotopic cisternography showed a pattern compatible with hypotension, without signs of fistulas. On spinal MR no spinal meningeal defects were seen. With conservative treatment the patient improved in a few days and the headache and diplopia disappeared. The absence of traumatism or spinal operations mean that the hypotension may be considered to be spontaneous. We discuss the CSF, neuroimaging and cisternography findings characteristic of the spontaneous intracranial hypotension syndrome. CONCLUSION: Unawareness of this syndrome, the particular neuroimaging changes and the usual CSF anomalies may lead to confusion over diagnosis, leading to the use of invasive techniques unsuitable for a condition which often has a good prognosis and in which the symptoms resolve in a few days or weeks with conservative treatment.

Abducens Nerve↗

PubMedDate not supplied

[Recurrent spontaneous carotid dissection].

INTRODUCTION: Arterial dissection is the cause of 20% of the stroke occurring in adults under the age of 45. The existence of recurrence has been discussed in recent studies, and the overall frequency estimated as 4% to 8%, with a risk of 1% per year. The course of the condition is usually oligosymptomatic, so that a high index of suspicion is necessary for diagnosis to be made. We consider that different connective tissue disorders and anomalies of the vascular wall predispose to dissection. It would seen reasonable to think that these same anomalies may lead to recurrence. However, this cannot always be demonstrated. A family history of dissection is also an important factor in recurrence. CLINICAL CASES: We present two cases of recurrent spontaneous dissection of the carotid artery from a series of 22 patients with dissection, during the period 1990-1997. In the first case, the second dissection occurred 15 days after the first and in the second case, seven months later. In both cases the recurrence was in the contra-lateral carotid artery. In the second case the vascular tree was noted to have been formed of ecstatic, tortuous vessels. CONCLUSIONS: Our series shows results similar to others published. In one of these, an underlying arteriopathy which predisposed to the condition was shown. Both followed satisfactory courses. In case 2 a high index of clinical suspicion was necessary, since the recurrence presented as headache alone.

Adult↗