[Anatomical variations of the middle cerebral artery: duplication and accessory artery. Implications in the treatment of acute stroke]. / Variantes anatomicas de la arteria cerebral media: duplicidad y arteria accesoria. Implicaciones en el tratamiento del ictus agudo.

INTRODUCTION: Less than half of all subjects display a normal configuration of the Circle of Willis, according to anatomical studies. Variations of the middle cerebral artery (MCA) such as duplication or accessory MCA are infrequent but nevertheless have important clinical implications. We report the case of two patients with these variations of the MCA and their repercussions in the management of acute stroke are discussed. CASE REPORTS: Case 1: a 53 year old male with a 2 hour history of sensory motor syndrome; a transcranial Doppler (TCD) scan revealed asymmetrical speeds in the MCA. Spontaneous perforation of the MCA was suspected and we therefore decided to perform a magnetic resonance angiography scan before administering fibrinolytics. The magnetic resonance angiography scan showed an accessory MCA lying ipsilateral to the lesion. We interpreted the anomalies in blood flow detected in the TCD recording as being secondary to this anatomical variation and not due to reperfusion. Following the magnetic resonance angiography study, the possibility of fibrinolysis was ruled out. The patient recovered the neurological deficit in a matter of hours. Case 2: a 21 year old female with headaches and transient hemiparesis, who was diagnosed as suffering from migraine with aura. Later, following another stroke, it was shown that the previous clinical symptoms had been secondary to intracranial dissection with embolism in the lenticulostriate arteries and ischemic infarction in that territory. A magnetic resonance angiography scan showed duplication of the ipsilateral MCA. CONCLUSIONS: The double vascularisation of the hemisphere in cases of anatomical duplication can give rise to strokes with a better progression and prognosis, despite the occlusion of one of the MCA. The presence of anatomical variations of the MCA can lead to mistaken interpretations of the transcranial Doppler scan and may affect decision making as regards the therapy to be employed in patients with acute stroke.

Variantes anatómicas de la arteria cerebral media: duplicidad y arteria accesoria. Implicaciones en el tratamiento del ictus agudo / Anatomical variations of the middle cerebral artery: duplication and accessory artery. Implications in the treatment of acute stroke

Introducción. La conformación normal del polígono de Willis aparece en menos de la mitad de los sujetos, según estudios anatómicos. Las variantes de la arteria cerebral media (ACM) como la duplicidad o la ACM accesoria son infrecuentes, aunque con implicaciones clínicas importantes. Se presentan dos pacientes con estas variantes de la ACM y se discute su repercusión en el manejo del ictus agudo. Casos clínicos. Caso 1: varón de 53 años, con síndrome sensitivo motor de dos horas de evolución, cuya ecografía Doppler transcraneal (EDTC) mostró una asimetría de velocidades en la ACM. Ante la sospecha de reperfusión espontánea de la ACM, se decidió practicar una angiorresonancia antes de administrar fibrinolíticos. La angiorresonancia mostró una ACM accesoria ipsilateral a la lesión. Se interpretó que las anomalías de flujo detectadas en la EDTC eran secundarias a esta variante anatómica y no a reperfusión. Tras el estudio de angiorresonancia se desestimó la fibrinólisis. El paciente recuperó el déficit neurológico en el plazo de horas. Caso 2: mujer de 21 años, con cefalea y hemiparesia transitoria diagnosticada de migraña con aura. Posteriormente, a raíz de otro ictus, se demostró que el cuadro clínico previo había sido secundario a disección intracraneal con embolismo de las arterias lenticuloestriadas e infarto isquémico en dicho territorio. La angiorresonancia demostró una duplicidad de la ACM ipsilateral. Conclusiones. La doble vascularización hemisférica en casos de duplicidad anatómica puede ocasionar ictus de mejor evolución y pronóstico, a pesar de la oclusión de una de las ACM. La presencia de variantes anatómicas de la ACM puede dar lugar a interpretaciones erróneas del estudio Doppler transcraneal y afectar a la decisión terapéutica en pacientes con ictus agudo (AU)

Introduction. Less than half of all subjects display a normal configuration of the circle of Willis, according to anatomical studies. Variations of the middle cerebral artery (MCA) such as duplication or accessory MCA are infrequent but nevertheless have important clinical implications. We report the case of two patients with these variations of the MCA and their repercussions in the management of acute stroke are discussed. Case reports. Case 1: a 53-year-old male with a 2-hour history of sensory-motor syndrome; a transcranial Doppler (TCD) scan revealed asymmetrical speeds in the MCA. Spontaneous perforation of the MCA was suspected and we therefore decided to perform a magnetic resonance angiography scan before administering fibrinolytics. The magnetic resonance angiography scan showed an accessory MCA lying ipsilateral to the lesion. We interpreted the anomalies in blood flow detected in the TCD recording as being secondary to this anatomical variation and not due to reperfusion. Following the magnetic resonance angiography study, the possibility of fibrinolysis was ruled out. The patient recovered the neurological deficit in a matter of hours. Case 2: a 21-year-old female with headaches and transient hemiparesis, who was diagnosed as suffering from migraine with aura. Later, following another stroke, it was shown that the previous clinical symptoms had been secondary to intracranial dissection with embolism in the lenticulostriate arteries and ischemic infarction in that territory. A magnetic resonance angiography scan showed duplication of the ipsilateral MCA. Conclusions. The double vascularisation of the hemisphere in cases of anatomical duplication can give rise to strokes with a better progression and prognosis, despite the occlusion of one of the MCA. The presence of anatomical variations of the MCA can lead to mistaken interpretations of the TCD scan and may affect decision-making as regards the therapy to be employed in patients with acute stroke (AU)

[Chloroquine-induced myopathy and neuropathy: progressive tetraparesis with areflexia that simulates a polyradiculoneuropathy. Two case reports]. / Miopatía y neuropatía inducida por cloroquina: tetraparesia progresiva con arreflexia que simula una polirradiculoneuropatía. A propósito de dos casos.

INTRODUCTION: Chloroquine is a drug that is widely used in rheumatology and occasionally prescribed in dermatology. From a neurotoxicological point of view, chloroquine can have effects on the peripheral nerves, muscles, neuromuscular junctions and the central nervous system. In this study we analyse the clinical, neurophysiological and anatomopathological findings in two patients with chloroquine induced neuromyopathy, which took the form of a polyradiculoneuropathy. CASE REPORTS: Case 1: a 75 year old female with rheumatoid arthritis treated with daily doses of 250 mg of chloroquine for four years. The patient visited because of several months history of predominantly proximal progressive tetraparesis with areflexia. Analytical tests and lumbar puncture were normal. Electromyogram (EMG): proximal myopathic and distal neuropathic patterns. Muscular biopsy: vacuolar myopathy with accumulations of phagolysosomes, lipids, lipofuscin, myelinic curvilinear bodies. Case 2: a 74 year old female with arthropathy treated with daily doses of 250 mg of chloroquine for nine months. The patient presented a progressive proximal paraparesis with generalised areflexia. Analytical tests and lumbar puncture were normal. EMG: mixed sensory motor polyneuropathy, myogenic pattern with high frequency discharges in the iliac psoas and a neurogenic pattern in the distal muscles. Muscular biopsy: vacuolar myopathy suggesting a myopathy due to chloroquine. After stopping treatment with this drug the patients progressed favourably. CONCLUSION: Chloroquine can induce a clinical pattern that suggests a polyradiculoneuropathy. It is important to establish a history of having taken this drug. If this is indeed the case, then an electromyographic study of the most proximal muscles should be performed in order to detect a myogenic pattern and the same exploration should be applied to the distal muscles to reveal a neurogenic pattern. The final diagnosis will be established by muscular biopsy.

Miopatía y neuropatía inducida por cloroquina: tetraparesia progresiva con arreflexia que simula una polirradiculoneuropatía. A propósito de dos casos / Chloroquine-induced myopathy and neuropathy: progressive tetraparesis with areflexia that simulates a polyradiculoneuropathy. Two case reports

Introducción. La cloroquina es un fármaco ampliamente utilizado en reumatología y, ocasionalmente, en dermatología. Desde el punto de vista neurotoxicológico, la cloroquina puede afectar a los nervios periféricos, a los músculos, a la unión neuromuscular y al sistema nervioso central. En el presente trabajo se analizan los hallazgos clínicos, neurofisiológicos y anatomopatológicos de dos pacientes con una neuromiopatía inducida por cloroquina, que se manifestaron como una polirradiculoneuropatía. Casos clínicos. Caso 1. Mujer de 75 años con artritis reumatoide tratada con cloroquina 250 mg/día durante cuatro años. Consultó por tetraparesia progresiva de predominio proximal de meses de evolución con arreflexia. Las pruebas analíticas y la punción lumbar fueron normales. Electromiograma (EMG): patrones miopáticos proximales y neuropáticos distales. Biopsia muscular: miopatía vacuolar con acúmulo de fagolisosomas, lípidos, lipofucsina, cuerpos mielínicos y curvilíneos. Caso 2. Mujer de 74 años con artropatía tratada con cloroquina 250 mg/día durante nueve meses. Presentó una paraparesia proximal progresiva con arreflexia universal. Las pruebas analíticas y la punción lumbar fueron normales. EMG: polineuropatia mixta sensitivomotora, patrón miógeno con descargas de alta frecuencia en psoas ilíaco y patrón neurógeno en los músculos distales. Biopsia muscular: miopatía vacuolar sugestiva de miopatía por cloroquina. Tras la retirada de la medicación presentaron una evolución favorable de la clínica. Conclusión. La cloroquina puede inducir un cuadro clínico sugestivo de polirradiculoneuropatía. Es importante interrogar sobre el antecedente de ingesta del fármaco. En caso positivo tiene interés el estudio electromiográfico de los músculos más proximales para detectar patrón miógeno y de los músculos distales para evidenciar patrón neurógeno. La biopsia muscular establecerá el diagnóstico definitivo (AU)

Chloroquine is a drug that is widely used in rheumatology and occasionally prescribed in dermatology. From a neurotoxicological point of view, chloroquine can have effects on the peripheral nerves, muscles, neuromuscular junctions and the central nervous system. In this study we analyse the clinical, neurophysiological and anatomopathological findings in two patients with chloroquine-induced neuromyopathy, which took the form of a polyradiculoneuropathy. Case reports. Case 1: a 75-year-old female with rheumatoid arthritis treated with daily doses of 250 mg of chloroquine for four years. The patient visited because of several months’ history of predominantly proximal progressive tetraparesis with areflexia. Analytical tests and lumbar puncture were normal. Electromyogram (EMG): proximal myopathic and distal neuropathic patterns. Muscular biopsy: vacuolar myopathy with accumulations of phagolysosomes, lipids, lipofuscin, myelinic curvilinear bodies. Case 2: a 74-year-old female with arthropathy treated with daily doses of 250 mg of chloroquine for nine months. The patient presented a progressive proximal paraparesis with generalised areflexia. Analytical tests and lumbar puncture were normal. EMG: mixed sensory-motor polyneuropathy, myogenic pattern with high frequency discharges in the iliac psoas and a neurogenic pattern in the distal muscles. Muscular biopsy: vacuolar myopathy suggesting a myopathy due to chloroquine. After stopping treatment with this drug the patients progressed favourably. Conclusion. Chloroquine can induce a clinical pattern that suggests a polyradiculoneuropathy. It is important to establish a history of having taken this drug. If this is indeed the case, then an electromyographic study of the most proximal muscles should be performed in order to detect a myogenic pattern and the same exploration should be applied to the distal muscles to reveal a neurogenic pattern. The final diagnosis will be established by muscular biopsy (AU)