18F-FDG PET/TC y RM funcional en un caso de afasia progresiva primaria logopénica cruzada / 18F-FDG PET/CT and functional MRI in a case of crossed logopenic primary progressive aphasia

La afasia progresiva primaria es un síndrome clínico secundario a la neurodegeneración de las áreas y redes neuronales involucradas en el lenguaje, habitualmente en el hemisferio izquierdo. El término «afasia cruzada» se refiere a una alteración del lenguaje como consecuencia de una lesión del hemisferio cerebral ipsilateral a la mano dominante. Presentamos el caso de una mujer diestra de 75 años con afasia progresiva primaria logopénica, con dificultad para encontrar palabras, de 2 años de evolución. La 18F-FDG PET/TC mostró un hipometabolismo temporoparietal derecho. Se realizó una RM funcional para caracterizar patrones de lateralización del lenguaje. Se observó un patrón de activación similar en ambos hemisferios y una menor activación de la esperada en el giro frontal inferior bilateral. Estos hallazgos apoyan que la afasia progresiva primaria logopénica no debería considerarse como una afectación de inicio en el hemisferio izquierdo, sino un síndrome caracterizado por una neurodegeneración asimétrica con preferencia por áreas y redes neuronales implicadas en el lenguaje (AU)

Primary progressive aphasia is a clinical syndrome caused by a neurodegeneration of areas and neural networks involved in language, usually in the left hemisphere. The term "crossed aphasia" denotes an acquired language dysfunction caused by a lesion in the hemisphere ipsilateral to the dominant hand. A case is presented on a 75-year-old right-handed woman with a logopenic variant of primary progressive aphasia with word-finding difficulties of 2 years onset. The 18F-FDG PET/CT showed right temporoparietal hypometabolism. A functional MRI scan was performed during a verb naming task in order to characterise language lateralisation patterns. A similar activation pattern was observed in both hemispheres, with less activation than expected in bilateral inferior frontal gyrus. These findings support that logopenic variant of primary progressive aphasia should not be considered as a neurodegeneration starting in the left brain hemisphere, but as a syndrome characterised by asymmetric neurodegeneration of brain regions and neural networks involved in language (AU)

18F-FDG PET/CT and functional MRI in a case of crossed logopenic primary progressive aphasia. / 18F-FDG PET/TC y RM funcional en un caso de afasia progresiva primaria logopénica cruzada.

Primary progressive aphasia is a clinical syndrome caused by a neurodegeneration of areas and neural networks involved in language, usually in the left hemisphere. The term "crossed aphasia" denotes an acquired language dysfunction caused by a lesion in the hemisphere ipsilateral to the dominant hand. A case is presented on a 75-year-old right-handed woman with a logopenic variant of primary progressive aphasia with word-finding difficulties of 2 years onset. The 18F-FDG PET/CT showed right temporoparietal hypometabolism. A functional MRI scan was performed during a verb naming task in order to characterise language lateralisation patterns. A similar activation pattern was observed in both hemispheres, with less activation than expected in bilateral inferior frontal gyrus. These findings support that logopenic variant of primary progressive aphasia should not be considered as a neurodegeneration starting in the left brain hemisphere, but as a syndrome characterised by asymmetric neurodegeneration of brain regions and neural networks involved in language.

Validación de la versión española del test Addenbrooke's Cognitive Examination III para el diagnóstico de demencia / Validation of the Spanish version of Addenbrooke's Cognitive Examination III for diagnosing dementia

Introducción: El Addenbrooke's Cognitive Examination (ACE) es un test de cribado para el diagnóstico de demencia. Recientemente, se ha desarrollado la tercera versión del test (ACE-III). El objetivo del estudio fue la traducción y adaptación del ACE-III al español y su validación. Material y métodos: El ACE-III fue traducido y adaptado al español. Se administró a un grupo de sujetos cognitivamente sanos y a pacientes con demencia leve de diferentes tipos en 2 centros españoles. Resultados: La consistencia interna del test (alfa de Cronbach = 0,927), la fiabilidad interevaluador (coeficiente de correlación intraclase = 0,976) y la fiabilidad test-retest (kappa = 0,995) fueron elevadas. Edad (r = –0,512) y escolaridad (r = 0,659) se correlacionaron significativamente con la puntuación total del test. La capacidad diagnóstica del ACE-III fue superior al Mini-Mental State Examination, especialmente en el grupo con mayor escolaridad. Se obtuvieron datos normativos por edad, y puntos de corte para la detección de demencia. Conclusiones: La versión española del test ACE-III es un instrumento válido para el diagnóstico de demencia, con una alta capacidad discriminatoria especialmente en pacientes con un mayor nivel educativo

Introduction: Addenbrooke's Cognitive Examination is a screening test used to diagnose dementia. The third edition of this test (ACE-III) was recently developed. The aim of this study was to translate and validate the ACE-III in Spanish. Methods: The ACE-III was translated and adapted to Spanish. It was then administered to a group of healthy subjects as well as a group of patients with different types of mild dementia treated in 2 hospitals in Spain. Results: Internal reliability (Cronbach's alpha = 0.927), inter-rater reliability (intraclass correlation coefficient = 0.976) and test-retest reliability (kappa 0.995) were excellent. Age (r = -0.512) and education (r = 0.659) showed a significant correlation with total test scores. The diagnostic accuracy of ACE-III was higher than that of the Mini-Mental State Examination, particularly for the group with the highest educational level. Researchers obtained normative data and cut-off points for the diagnosis of dementia. Conclusions: The Spanish version of the ACE-III is a reliable and valid test for diagnosing dementia. Its diagnostic accuracy is high, especially in patients with a higher level of education

Afasia progresiva logopénica asociada a enfermedad de Parkinson idiopática / Logopenic progressive aphasia associated with idiopathic Parkinson's disease

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Topography of primitive reflexes in dementia: an F-18 fluorodeoxyglucose positron emission tomography study.

BACKGROUND AND PURPOSE: Although primitive reflexes (PRs) are inhibited during the first years of childhood, they may reappear with brain injury. PRs have been linked to frontal lobe dysfunction, but their precise topography has not yet been defined. The purpose of this study was to map which regions of the brain display a reduced glucose metabolism in patients with cognitive impairment and PRs. METHODS: A prospective study was conducted to evaluate PRs in a group of patients assessed due to suspected cognitive decline. Neurological and neuropsychological examinations and (18) F-fluorodeoxyglucose positron emission tomography fused with computerized tomography were performed. Voxel-based brain mapping analysis by means of statistical parametric mapping was used to compare patients with and without PRs. RESULTS: The study included 99 patients (33 diagnosed with Alzheimer's disease, 33 on the frontotemporal dementia spectrum and 33 with other diagnoses). Mean age was 71 ± 9.7 years; time since symptom onset was 3.6 ± 2.9 years. At least one PR was observed in 43 cases (43.4% of the whole sample; 48.5% in the Alzheimer disease group, 63.6% in frontotemporal dementia and 18.2% in the group with other diagnoses). The group of patients with PRs exhibited a decreased cerebral metabolism in the bilateral superior frontal gyri (Brodmann area 6), bilateral putamina and thalami. CONCLUSIONS: The presence of PRs was associated with hypometabolism at the superior frontal gyrus and putamen. This suggests that dysfunction in the corticostriatal motor circuit (supplementary motor area-putamen-thalamus) may constitute the anatomical basis of the recurrence of PRs.

Demencia frontotemporal variante conductual: biomarcadores, una aproximación a la enfermedad / Biomarkers: A new approach to behavioural variant frontotemporal dementia

Introducción: Las degeneraciones lobares frontotemporales (DLFT) son un grupo de patologías moleculares que se definen en función de la proteína acumulada en el sistema nervioso central. La demencia frontotemporal variante conductual (DFT vc) es el síndrome clínico de presentación más frecuente. Los avances realizados en los últimos anos han contribuido a un mayor conocimiento de esta entidad, que puede ser el modo de presentación de diferentes enfermedades neurodegenerativas. Desarrollo: Se revisa la correlación entre clínica, patología y genética de las DLFT, en especial de la DFT vc, así como los principales biomarcadores de la enfermedad. La anatomía patológica de la DFT vc es muy variada, sin mostrar asociación significativa con ningún subtipo histopatológico concreto. Entre los biomarcadores disponibles, destacan la neuroimagen anatómica y funcional, los biomarcadores analíticos y la genética. Se están disenando fármacos dirigidos contra dianas moleculares concretas implicadas en la patogenia de las DLFT. Conclusiones: La DFT vc es una causa frecuente de demencia. De entre todas las variantes clínicas de las DLFT, es en la que resulta más difícil establecer una relación clínico-patológica. El uso de biomarcadores puede ayudar a predecir la anatomía patológica subyacente, lo que junto al desarrollo de fármacos ligando-específicos ofrece nuevas posibilidades terapéuticas

Introduction: Lobar frontotemporal degeneration (FTLD) encompasses a group of molecular disease defined by the deposition of an abnormal protein in the central nervous system. Behavioural variant frontotemporal dementia (bvFTD) is the most frequent clinical presentation of FTLD. The past two decades of research have contributed to a better understanding of this entity, which may be the first manifestation in many different neurodegenerative disorders. Development: We reviewed correlations between clinical, pathological, and genetic findings and the main disease biomarkers of FTLD, with particular interest in bvFTD. Anatomical pathology findings in FTLD are heterogeneous and the syndrome is not associated with any one specific histopathological type. Promising available biomarkers include structural and functional neuroimaging techniques and biochemical and genetic biomarkers. Disease-modifying drugs designed for specific molecular targets that are implicated in FTLD pathogenesis are being developed. Conclusions: BvFTD is a frequent cause of dementia. Of all the clinical variants of FTLD, behavioural variant is the one in which establishing a correlation between clinical and pathological signs is the most problematic. A biomarker evaluation may help predict the underlying pathology; this approach, in conjunction with the development of disease-modifying drugs, offers new therapeutic possibilities

Biomarkers: a new approach to behavioural variant frontotemporal dementia.

INTRODUCTION: Lobar frontotemporal degeneration (FTLD) encompasses a group of molecular disease defined by the deposition of an abnormal protein in the central nervous system. Behavioural variant frontotemporal dementia (bvFTD) is the most frequent clinical presentation of FTLD. The past two decades of research have contributed to a better understanding of this entity, which may be the first manifestation in many different neurodegenerative disorders. DEVELOPMENT: We reviewed correlations between clinical, pathological, and genetic findings and the main disease biomarkers of FTLD, with particular interest in bvFTD. Anatomical pathology findings in FTLD are heterogeneous and the syndrome is not associated with any one specific histopathological type. Promising available biomarkers include structural and functional neuroimaging techniques and biochemical and genetic biomarkers. Disease-modifying drugs designed for specific molecular targets that are implicated in FTLD pathogenesis are being developed. CONCLUSIONS: BvFTD is a frequent cause of dementia. Of all the clinical variants of FTLD, behavioural variant is the one in which establishing a correlation between clinical and pathological signs is the most problematic. A biomarker evaluation may help predict the underlying pathology; this approach, in conjunction with the development of disease-modifying drugs, offers new therapeutic possibilities.

Validation of the Spanish version of Addenbrooke's Cognitive Examination III for diagnosing dementia.

INTRODUCTION: Addenbrooke's Cognitive Examination is a screening test used to diagnose dementia. The third edition of this test (ACE-III) was recently developed. The aim of this study was to translate and validate the ACE-III in Spanish. METHODS: The ACE-III was translated and adapted to Spanish. It was then administered to a group of healthy subjects as well as a group of patients with different types of mild dementia treated in 2 hospitals in Spain. RESULTS: Internal reliability (Cronbach's alpha = 0.927), inter-rater reliability (intraclass correlation coefficient = 0.976) and test-retest reliability (kappa 0.995) were excellent. Age (r = -0.512) and education (r = 0.659) showed a significant correlation with total test scores. The diagnostic accuracy of ACE-III was higher than that of the Mini-Mental State Examination, particularly for the group with the highest educational level. Researchers obtained normative data and cut-off points for the diagnosis of dementia. CONCLUSIONS: The Spanish version of the ACE-III is a reliable and valid test for diagnosing dementia. Its diagnostic accuracy is high, especially in patients with a higher level of education.

Demencia frontotemporal variante conductual: aproximación clínica y terapéutica / Behavioural variant frontotemporal dementia: Clinical and therapeutic approaches

Introducción: La variante conductual de la demencia frontotemporal (DFT vc) es el síndrome clínico más frecuente de las demencias frontotemporales (DFT) y se caracteriza por una alteración progresiva de la personalidad y la conducta. En las últimas 2 décadas, los avances en biología molecular y genética han contribuido a un mayor conocimiento de esta entidad, que puede ser el modo de presentación de diferentes enfermedades neurodegenerativas. Desarrollo: Se revisan los principales aspectos epidemiológicos, clínicos, diagnósticos y terapéuticos de la DFT vc. La mayoría de los casos son esporádicos, iniciándose en torno a los 58 años de media. Los criterios diagnósticos vigentes establecen 3 niveles de certeza diagnóstica: posible, probable y definitivo. El diagnóstico clínico se basa en la anamnesis detallada de familiares, complementada con la realización de test neuropsicológicos dirigidos. Hasta la fecha, los tratamientos empleados son solo sintomáticos y de eficacia controvertida. Se están diseñando fármacos dirigidos contra dianas moleculares específicas implicadas en la patogenia de las degeneraciones lobares frontotemporales. Conclusiones: La DFT vc es una causa frecuente de demencia. Se trata de un síndrome amplio, heterogéneo desde el punto de vista histopatológico y biomolecular. La definición de subtipos clínicos y la identificación de biomarcadores podrían ayudar a predecir la afección subyacente,lo que junto con el desarrollo de fármacos dirigidos contra dianas moleculares ofrece nuevas posibilidades terapéuticas

Introduction: Behavioural variant frontotemporal dementia (bvFTD) is the most frequent presentation in the clinical spectrum of frontotemporal dementia (FTD) and it is characterised by progressive changes in personality and conduct. Major breakthroughs in molecular biology and genetics made during the last two decades have lent us a better understanding of this syndrome, which may be the first manifestation in many different neurodegenerative diseases. Development: We reviewed the main epidemiological, clinical, diagnostic and therapeutic aspects of bvFTD. Most cases manifest sporadically and the average age of onset is 58 years. Current criteria for bvFTD propose three levels of diagnostic certainty: possible, probable, and definite. Clinical diagnosis is based on a detailed medical history provided by family members and caregivers, in conjunction with neuropsychological testing. Treatments which have been used in bvFDT to date are all symptomatic and their effectiveness is debatable. New drugs designed for specific molecular targets that are implicated in frontotemporal lobar degeneration are being developed. Conclusions: BvFDT is a frequent cause of dementia. It is a non-specific syndrome associated with heterogeneous histopathological and biomolecular findings. The definition of clinical subtypes complemented by biomarker identification may help predict the underlying pathology. This knowledge, along with the development of drugs designed for molecular targets, will offer new treatment possibilities

Behavioural variant frontotemporal dementia: clinical and therapeutic approaches.

INTRODUCTION: Behavioural variant frontotemporal dementia (bvFTD) is the most frequent presentation in the clinical spectrum of frontotemporal dementia (FTD) and it is characterised by progressive changes in personality and conduct. Major breakthroughs in molecular biology and genetics made during the last two decades have lent us a better understanding of this syndrome, which may be the first manifestation in many different neurodegenerative diseases. DEVELOPMENT: We reviewed the main epidemiological, clinical, diagnostic and therapeutic aspects of bvFTD. Most cases manifest sporadically and the average age of onset is 58 years. Current criteria for bvFTD propose three levels of diagnostic certainty: possible, probable, and definite. Clinical diagnosis is based on a detailed medical history provided by family members and caregivers, in conjunction with neuropsychological testing. Treatments which have been used in bvFDT to date are all symptomatic and their effectiveness is debatable. New drugs designed for specific molecular targets that are implicated in frontotemporal lobar degeneration are being developed. CONCLUSIONS: BvFDT is a frequent cause of dementia. It is a non-specific syndrome associated with heterogeneous histopathological and biomolecular findings. The definition of clinical subtypes complemented by biomarker identification may help predict the underlying pathology. This knowledge, along with the development of drugs designed for molecular targets, will offer new treatment possibilities.

Discinesia orofacial aguda inducida por fenitoína / Phenytoin-induced acute orofacial dyskinesia

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Mielitis longitudinal como forma de presentación de neurosarcoidosis / Longitudinal myelitis as the presenting symptom of neurosarcoidosis

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[Meralgia paraesthetica: a report on a series of 140 cases]. / Meralgia parestésica: a propósito de una serie de 140 casos.

INTRODUCTION: Meralgia paraesthetica is a pathology that is frequently seen in visits to extra-hospital neurology services. Nevertheless, the diagnosis, treatment and prognosis of this condition remain somewhat unclear. PATIENTS AND METHODS: A retrospective study was conducted involving 140 patients. Data were collected concerning demographic aspects, clinical picture, diagnostic study, aetiology, treatment and progression. RESULTS: There was a predominance of males, with a mean age of 54 years. The mean follow-up time was 25 months. The symptoms that were reported were as follows: numbness, burning pain, tingling or prickling in the nerve territory. Hypaesthesia was the most frequent sign found in the examination. History of another compressive neuropathy was present in 13.6% of patients. The diagnosis was based on the patient record and the neurological examination. The neurophysiological study and complementary tests were reserved for atypical cases. The most common causation was spontaneous and only three cases were found to be secondary to a structural lesion. A third of the patients were receiving pharmacological treatment. Although the clinical picture was benign, in most cases it tended to become chronic. Patients treated pharmacologically did not show a significant improvement in comparison to those who were not given treatment. The most important data for forecasting improvement of the clinical picture were the identification and correction of the factors precipitating compression of the nerve. CONCLUSIONS: Meralgia paraesthetica is a frequent, benign pathology but with a tendency to become chronic that responds poorly to pharmacological treatment. It is important to identify and correct mechanical factors and only in exceptional cases is it secondary to a structural lesion.

Meralgia parestésica: a propósito de una serie de 140 casos / Meralgia Paraesthetca: a report on a series of 140 cases

Introducción. La meralgia parestésica es una patología frecuente en la consulta de neurología extrahospitalaria. Apesar de ello, el diagnóstico, tratamiento y pronóstico de este cuadro no están bien establecidos. Pacientes y métodos. Estudioretrospectivo de 140 pacientes. Se recogen datos demográficos, clínica, estudio diagnóstico, etiología, tratamiento y evolución.Resultados. Hubo un predominio masculino, con una mediana de 54 años. El seguimiento medio fue de 25 meses. Lossíntomas narrados fueron: acorchamiento, dolor urente, hormigueo o pinchazos en el territorio nervioso. En la exploración sehalló hipoestesia como signo más frecuente. Hubo historia de otra neuropatía compresiva en el 13,6%. El diagnóstico se basóen la historia clínica y la exploración neurológica. El estudio neurofisiológico y las pruebas complementarias se reservaronpara casos atípicos. La etiología más frecuente fue la espontánea, y se hallaron sólo tres casos secundarios a lesión estructural.Un tercio de los pacientes recibió tratamiento farmacológico. Aunque el cuadro fue benigno, en la mayoría tendióa cronificarse. Los pacientes tratados farmacológicamente no mostraron una mejoría significativa frente a los que no recibierontratamiento. El dato pronóstico más importante para la mejoría del cuadro fue la identificación y corrección de los factoresdesencadenantes de compresión del nervio. Conclusiones. La meralgia parestésica es una patología frecuente, benigna,pero con tendencia a cronificarse, en la que es importante identificar y corregir factores mecánicos, con pobre respuesta altratamiento farmacológico, y sólo en casos excepcionales secundaria a lesión estructural (AU)

Introduction. Meralgia paraesthetica is a pathology that is frequently seen in visits to extra-hospital neurologyservices. Nevertheless, the diagnosis, treatment and prognosis of this condition remain somewhat unclear. Patients andmethods. A retrospective study was conducted involving 140 patients. Data were collected concerning demographic aspects,clinical picture, diagnostic study, aetiology, treatment and progression. Results. There was a predominance of males, with amean age of 54 years. The mean follow-up time was 25 months. The symptoms that were reported were as follows: numbness,burning pain, tingling or prickling in the nerve territory. Hypaesthesia was the most frequent sign found in the examination.History of another compressive neuropathy was present in 13.6% of patients. The diagnosis was based on the patient recordand the neurological examination. The neurophysiological study and complementary tests were reserved for atypical cases. Themost common causation was spontaneous and only three cases were found to be secondary to a structural lesion. A third of thepatients were receiving pharmacological treatment. Although the clinical picture was benign, in most cases it tended to becomechronic. Patients treated pharmacologically did not show a significant improvement in comparison to those who were not giventreatment. The most important data for forecasting improvement of the clinical picture were the identification and correction ofthe factors precipitating compression of the nerve. Conclusions. Meralgia paraesthetica is a frequent, benign pathology butwith a tendency to become chronic that responds poorly to pharmacological treatment. It is important to identify and correctmechanical factors and only in exceptional cases is it secondary to a structural lesion. (AU)

Neuralgia supraorbitaria: una alternativa intervencionista. Réplica / Supraorbital neuralgia: an interventionist alternative. Reply

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Neuralgia supraorbitaria postraumática: una entidad benigna / Post-traumatic supraorbital neuralgia: a benign condition

Introducción. La neuralgia supraorbitaria es una entidad de reciente descripción. La mayor parte de los pacientes publicados sufre neuralgias idiopáticas, crónicas, de difícil tratamiento, que en ocasiones requieren cirugía de liberación del nervio. Presentamos nuestra experiencia en pacientes con una variante de esta neuralgia de causa conocida, aparición frecuente y pronóstico benigno. Casos clínicos. Estudiamos cinco pacientes, cuatro mujeres y un varón de 55 años de edad media (rango: 29-69 años). Todos sufrieron un traumatismo directo banal sobre la región frontal, de causa diversa. Cuatro desarrollaron un dolor continuo, de tipo pinchazo o quemazón, tres un dolor paroxístico y uno prurito. No hubo manifestaciones autonómicas. Todos presentaron una exploración de la sensibilidad anómala en el territorio afectado, con hipoestesia tactil, hiperalgesia o alodinia y signo de Tinel positivo. Las pruebas de neuroimagen fueron normales. Dos recibieron tratamiento con gabapentina y amitriptilina. Uno fue tratado con un bloqueo anestésico, con una mejoría transitoria. Tres no recibieron tratamiento alguno. Tras un año de seguimiento, todos mejoraron y tres quedaron sin dolor, si bien en todos persistieron alteraciones sensitivas. Conclusiones. La neuralgia supraorbitaria postraumática es una entidad frecuente, aunque probablemente infradiagnosticada. Presenta características clínicas y evolutivas particulares que la diferencian de la neuralgia supraorbitaria idiopática. Suele tener una buena evolución y una respuesta favorable al tratamiento sintomático, si es que llega a requerir alguno

Introduction. Supraorbital neuralgia has only recently been described. Most of the cases reported involve patients suffering from chronic idiopathic neuralgias that are difficult to treat and sometimes require surgery to release the nerve. We present our experience in patients with a variant of this neuralgia which has a known causation, is commonly seen and has a benign prognosis. Case reports. We studied five patients, four females and one male, with a mean age of 55 years (range: 29-69 years). They had all suffered direct banal traumatic injury to the frontal region due to different causes. Four of them developed continuous, piercing or burning-type pain; three of them had paroxysmal pain and one had itching. There were no autonomic manifestations. All of them were found to be abnormally sensitive in the affected area, with tactile hypaesthesia, hyperalgesia or allodynia and a positive Tinel’s sign. Neuroimaging tests were normal. Two patients were treated with gabapentin and amitriptyline. One was treated with an anaesthetic blockade, which afforded temporary relief. Three of them received no treatment at all. After one year of follow-up, all of them had improved and three were no longer in pain, although sensory alterations persisted in all cases. Conclusions. Post-traumatic supraorbital neuralgia is a frequent condition, although it is probably underdiagnosed. It has its own characteristic clinical and developmental features that distinguish it from idiopathic supraorbital neuralgia. Progress is usually good and it responds favourably to symptomatic treatment, if needed

[Post-traumatic supraorbital neuralgia: a benign condition]. / Neuralgia supraorbitaria postraumática: una entidad benigna.

INTRODUCTION: Supraorbital neuralgia has only recently been described. Most of the cases reported involve patients suffering from chronic idiopathic neuralgias that are difficult to treat and sometimes require surgery to release the nerve. We present our experience in patients with a variant of this neuralgia which has a known causation, is commonly seen and has a benign prognosis. CASE REPORTS: We studied five patients, four females and one male, with a mean age of 55 years (range: 29-69 years). They had all suffered direct banal traumatic injury to the frontal region due to different causes. Four of them developed continuous, piercing or burning-type pain; three of them had paroxysmal pain and one had itching. There were no autonomic manifestations. All of them were found to be abnormally sensitive in the affected area, with tactile hypaesthesia, hyperalgesia or allodynia and a positive Tinel's sign. Neuroimaging tests were normal. Two patients were treated with gabapentin and amitriptyline. One was treated with an anaesthetic blockade, which afforded temporary relief. Three of them received no treatment at all. After one year of follow-up, all of them had improved and three were no longer in pain, although sensory alterations persisted in all cases. CONCLUSIONS: Post-traumatic supraorbital neuralgia is a frequent condition, although it is probably underdiagnosed. It has its own characteristic clinical and developmental features that distinguish it from idiopathic supraorbital neuralgia. Progress is usually good and it responds favourably to symptomatic treatment, if needed.