A 62-year-old patient at diagnosis, with no previous history of interest, non-diabetic, hypertensive, obese and menopause ten years earlier.
She was diagnosed with left breast carcinoma in March 2002, after performing a left radical mastectomy and ipsilateral axillary lymphadenectomy.
The histological result was ductal carcinoma of the breast, 14 mm, with metastatic disease in 2 of 7 lymph nodes isolated, with positive axillary permeation and positive axillary receptors immunohistochemistry.
It was then staged as pT1cN1biM0 (stage IIA).
He underwent polychemotherapy with a regimen of fluoracil, cyclophosphamide and 4-epirubicin (FEC), completing six cycles and subsequently continued on monotherapy (tamoxifen 20 mg daily).
In February 2003 she began with self-limiting holocraneal headaches and dizziness.
There were no neurological alterations on examination or other accompanying symptoms.
A cranial computerized axial tomography (CAT) revealed a right intraaxial cerebellar lesion, confirmed by magnetic resonance imaging (MRI) of the brain, with a glinic component of 4 cm in size.
An extension study was carried out, with a complete TAC of thorax-abdomen, mammogram and bone scintigraphy without evidence of disease; the values of asymmetry were normal, renal and hepatic function, with tumor markers.
It was decided to perform a craniotomy with complete exeresis of the described lesion, being the histological diagnosis of metastasis of breast carcinoma, with disease-free borders.
Two weeks after the intervention, the patient complained of pain with muscle characteristics in the lower limbs and hip, with progressive difficulty in walking, easy fatigue and inability to stand from bed, with significant paresthesia.
He presented behavioral changes, memory loss and episodes of confusion.
On physical examination, ataxia was observed, with a slight decrease in muscle strength in the lower limbs, especially proximal, with no alteration in osteotendinous reflexes or sensitivity, normal cranial nerves and no nystagmus.
Analgesic treatment, second line therapy with aromatase inhibitor, was initiated and cranial radiotherapy was planned.
Symptoms partially resolved, starting with episodes of flushing, profuse sweating and constipation.
A new study was carried out by means of cerebral and spinal examinations, not including spinal cord lesions, and only post-surgical changes in the right cerebellum and basal ganglia region, with minimal non-pathological enhancement after administration of MRI.
Holocrane radiotherapy was initiated to treat the surgery.
Tumor markers began to elevate slightly, with normal carcinoembryonic antigen (CEA), normal total antigen (CEA) and CA1305.3 IU/ml; elevated lactate-dehydrogenase (LDH) levels.
The neurophysiological study showed an evident miasteniform pattern of suicidal activity, consistent with Lambert-Eaton syndrome, with absence of denervative activity, myopic or medullary process.
We started steroid treatment at high doses of dexamethasone and programmed treatment with weekly plasmapheresis.
However, the patient continued with progressive clinical symptoms of occipital headache, increased asthenia, muscle weakness, bilateral ptosis, severe constipation due to intestinal paresis, temporo-spatial disorientation and plasmapheresis, with no response.
Brain MRI showed no parenchymal or surgical changes.
Lumbar puncture showed only mild hyperproteinorrhachia.
Later he suffered greater deterioration of superior functions with complete temporo-spatial disorientation and psychotic alterations, dysarthria and bpsychia, until he was in a coma situation.
Tumor markers continued to increase with CA 15.3 UI/ml, decreasing LDH to normal values.
The immunological study revealed an elevation of antineutrophil antibodies typical of nonspecific autoimmune diseases (ANCAp) (confirmed by PCR technique); negativity for the anti-acetylcholine receptor antibody was also negative.
She received chemotherapy treatment with taxanes and died in May 2003, several days in coma.
