A Historical Review of Headaches: Who First Described Them and When did This Occur?

BACKGROUND: Headache is as old as human history and has been able to report, and the first descriptions were found in Greece and Mesopotamia. OBJECTIVE: Our objective was to know the date of the first description of ICHD-3 headaches, with their respective author. METHODS: We searched for articles that addressed the historical aspects of primary and secondary headaches and painful cranial neuropathies. RESULTS: Twenty-seven different headaches were analyzed according to the occurrence of their first description, with the respective author and country of origin. CONCLUSIONS: The knowledge of the first description of ICHD-3 headaches, with their respective author, showed us how and when the different headaches appeared over the years.

Pathological classification of equine recurrent laryngeal neuropathy.

Recurrent Laryngeal Neuropathy (RLN) is a highly prevalent and predominantly left-sided, degenerative disorder of the recurrent laryngeal nerves (RLn) of tall horses, that causes inspiratory stridor at exercise because of intrinsic laryngeal muscle paresis. The associated laryngeal dysfunction and exercise intolerance in athletic horses commonly leads to surgical intervention, retirement or euthanasia with associated financial and welfare implications. Despite speculation, there is a lack of consensus and conflicting evidence supporting the primary classification of RLN, as either a distal ("dying back") axonopathy or as a primary myelinopathy and as either a (bilateral) mononeuropathy or a polyneuropathy; this uncertainty hinders etiological and pathophysiological research. In this review, we discuss the neuropathological changes and electrophysiological deficits reported in the RLn of affected horses, and the evidence for correct classification of the disorder. In so doing, we summarize and reveal the limitations of much historical research on RLN and propose future directions that might best help identify the etiology and pathophysiology of this enigmatic disorder.

Cranial Neuralgias.

Advances in diagnostic modalities have improved the understanding of the pathophysiology of neuropathic pain involving head and face. Recent updates in nomenclature of cranial neuralgias and facial pain have rationalized accurate diagnosis. Clear diagnosis and localization of pain generators are paramount, leading to better use of medical and targeted surgical treatments.

[Changes introduced into the recent International Classification of Headache Disorders: ICHD-III beta classification]. / Novedades en la reciente Clasificacion Internacional de las Cefaleas: clasificacion ICHD-III beta.

INTRODUCTION: The International Headache Society (IHS) has published the third edition of the International Classification of Headache Disorders (ICHD-III beta), the most commonly used guide to diagnosing headaches in the world. AIMS: To review the recent additions to the guide, to explain the new entities that appear in it and to compare the conditions that have had their criteria further clarified against the criteria in the previous edition. DEVELOPMENT: We have recorded a large number of clarifications in the criteria in practically all the headaches and neuralgias in the classification, but the conditions that have undergone the most significant clarifications are chronic migraine, primary headache associated with sexual activity, short-lasting unilateral neuralgiform headache attacks, new daily persistent headache, medication-overuse headache, syndrome of transient headache and neurological deficits with cerebrospinal fluid lymphocytosis. The most notable new entities that have been incorporated are external-compression headache, cold-stimulus headache, nummular headache, headache attributed to aeroplane travel and headache attributed to autonomic dysreflexia. Another point to be highlighted is the case of the new headaches (still not considered entities in their own right) included in the appendix, some of the most noteworthy being epicrania fugax, vestibular migraine and infantile colic. CONCLUSIONS: The IHS recommends no longer using the previous classification and changing over to the new classification (ICHD-III beta) in healthcare, teaching and research, in addition to making this new guide as widely known as possible.

TITLE: Novedades en la reciente Clasificacion Internacional de las Cefaleas: clasificacion ICHD-III beta.Introduccion. La Sociedad Internacional de Cefaleas (IHS) ha publicado la tercera edicion de la Clasificacion Internacional de las Cefaleas (ICHD-III beta), la guia diagnostica de las cefaleas mas utilizada en el mundo. Objetivo. Revisar las recientes aportaciones de la guia, explicando las nuevas entidades que en ella aparecen y comparando las entidades que han matizado sus criterios con sus criterios de la edicion precedente. Desarrollo. Hemos registrado multitud de matices en los criterios de practicamente todas las cefaleas y neuralgias de la clasificacion, pero las entidades que han experimentado mas matizaciones trascendentales son la migraña cronica, la cefalea asociada exclusivamente a la actividad sexual, las cefaleas neuralgiformes unilaterales de breve duracion, la cefalea diaria persistente de novo, la cefalea por abuso de medicacion sintomatica, el sindrome de cefalea y deficits neurologicos transitorios con pleocitosis linfocitaria. Las entidades nuevas mas destacables que se han incorporado son las cefaleas por presion externa, las cefaleas por crioestimulo, la cefalea numular, la cefalea atribuida a vuelos de avion y la cefalea atribuida a disreflexia autonomica. Tambien cabe destacar las nuevas cefaleas, aun no consideradas como entidades, que se incorporan al apendice, entre las que destacan la epicranea fugax, la migraña vestibular y los colicos infantiles. Conclusiones. La IHS recomienda utilizar ya la nueva clasificacion (ICHD-III beta), prescindiendo de la anterior clasificacion, en la asistencia, la docencia y la investigacion, asi como hacer la maxima difusion de esta nueva guia.

Corneal nerve alterations in different stages of Fuchs' endothelial corneal dystrophy: an in vivo confocal microscopy study.

PURPOSE: To analyze potential alterations in corneal nerve morphology and function in different stages of Fuchs' endothelial corneal dystrophy (FECD). METHODS: Thirty eyes with FECD underwent in vivo confocal microscopy using the Heidelberg Retina Tomograph II (HRT II; Heidelberg Engineering, Heidelberg, Germany) and the Rostock Cornea Module (RCM) to quantify the morphology of the central subbasal corneal nerve plexus (total nerve length, total nerve number, number of main nerve trunks, number of nerve branches) as well as esthesiometry (using the Cochet-Bonnet esthesiometer) of the central cornea to determine central corneal sensation as a measure of nerve function. Findings were correlated with an age-matched control group of 30 healthy individuals. Comparisons to biomicroscopical stage of FECD, visual acuity and central corneal thickness were performed using Spearman correlation. RESULTS: Depending on slit-lamp examination, all 30 eyes were classified into FECD stage 1-4 (stage 1: six eyes; stage 2: 15 eyes; stage 3: six eyes; stage 4: three eyes). Total nerve length (ρ = -0.8, p < 0.001), total nerve number (ρ = -0.7, p < 0.001), number of main nerve trunks (ρ = -0.6, p < 0.001), and number of nerve branches (ρ = -0.7, p < 0.001) decreased significantly with increasing FECD stages. Comparing to the visual acuity, significant positive correlations were found for total nerve length (ρ = 0.5, p = 0.012), total nerve number (ρ = 0.5, p = 0.005), number of main nerve trunks (ρ = 0.4, p = 0.017), and number of nerve branches (ρ = 0.5, p = 0.009). With central corneal thickness, there were significant inverse correlations for total nerve length (ρ = -0.6, p = 0.001), total nerve number (ρ = -0.5, p = 0.012), number of main nerve trunks (ρ = -0.4, p = 0.015), and number of nerve branches (ρ = -0.4, p = 0.017). Central corneal sensation was full in all FECD stage 1, stage 2 and stage 3 eyes, but mildly reduced in FECD stage 4 eyes. CONCLUSIONS: Increasing severity of Fuchs' endothelial corneal dystrophy (FECD) is concurrent with marked attenuation of the density, as well as mild diminishment of the function, of the subbasal corneal nerve plexus in late stage of the disease.

Anatomic considerations, nomenclature, and advanced cross-sectional imaging techniques for visualization of the cranial nerve segments by MR imaging.

Various methods of cross-sectional imaging are used for visualization of the cranial nerves, relying heavily on MR imaging. The success of the MR imaging sequences for visualization of cranial nerves depends on their anatomic context at the point of evaluation. The heterogeneity of opinion regarding optimal evaluation of the cranial nerves is partly a function of the complexity of cranial nerve anatomy. A variety of approaches are advocated and variations in equipment and terminology cloud the field. This article proposes a segmental classification and corresponding nomenclature for imaging evaluation of the cranial nerves and reviews technical considerations and applicable literature.

[Diabetic neuropathies: clinical sub-types, early detection, and asking help from neurologist]. / Diabetische Neuropathien: Klinische Manifestationsformen, Früherkennung und Zuweisung zu einem Neurologen.

In diabetes mellitus, it is expected to see a common, mainly sensitive, distal symmetrical polyneuropathy (DPN) involving a large proportion of diabetic patients according to known risk factors. Several other diabetic peripheral neuropathies are recognized, such as dysautonomia and multifocal neuropathies including lumbosacral radiculoplexus and oculomotor palsies. In this review, general aspects of DPN and other diabetic neuropathies are examined, and it is discussed why and how the general practitioner has to perform a yearly examination. At the present time, some consensus emerge to ask help from neurologist when faced to other forms of peripheral neuropathies than distal symmetrical DPN.

Cranial neuralgias: from physiopathology to pharmacological treatment.

Cranial neuralgias are paroxysmal painful disorders of the head characterised by some shared features such as unilaterality of symptoms, transience and recurrence of attacks, superficial and "shock-like" quality of pain and the presence of triggering factors. Although rare, these disorders must be promptly recognised as they harbour a relatively high risk for underlying compressive or inflammatory disease. Nevertheless, misdiagnosis is frequent. Trigeminal and glossopharyngeal neuralgias are sustained in most cases by a neurovascular conflict in the posterior fossa resulting in a hyperexcitability state of the trigeminal circuitry. If the aetiology of trigeminal neuralgia (TN) and other typical neuralgias must be brought back to the peripheral injury, their pathogenesis could involve central allodynic mechanisms, which, in patients with inter-critical pain, also engage the nociceptive neurons at the thalamic-cortical level. Currently available medical treatments for TN and other cranial neuralgias are reviewed.

Multiple cranial nerve palsies: analysis of 979 cases.

BACKGROUND: To my knowledge, no large series of multiple cranial neuropathies is available. OBJECTIVES: To examine the seats and causes of multiple cranial neuropathies in a large group of inpatients. DESIGN: Personal case series. SETTING: Wards of a large municipal hospital and affiliated rehabilitation hospital. PATIENTS: A consecutive series of 979 unselected inpatients with simultaneous or serial involvement of 2 or more different cranial nerves. RESULTS: Cranial nerves VI (565 cases), VII (466 cases), V (353 cases), and III (339 cases) were most commonly affected. The locations and causes were diverse, with cavernous sinus (252 cases), brainstem (217 cases), and individual nerves (182 cases) being the most frequent sites, and tumor (305 cases), vascular disease (128 cases), trauma (128 cases), infection (102 cases), and the Guillain-Barré and Fisher syndromes (91 cases total) being the most frequent causes. Recurrent cranial neuropathy was uncommon (43 cases, 106 episodes, 136 nerves), with diabetes mellitus (14 cases), self-limited unknown causes (14 cases), and idiopathic cavernous sinusitis (10 cases) being the usual causes. CONCLUSION: While the locations and causes of multiple cranial neuropathy are highly diverse, the fact that tumor composes more than one quarter of cases places a premium on prompt diagnosis.

Isolated cranial neuropathy associated with anti-glycolipid antibodies.

We describe seven patients with isolated cranial neuropathy in whom serum anti-glycolipid antibodies were detected. Trigeminal sensory neuropathy was found in four patients, who had exhibited symptoms for 2 months to 4 years. The other three patients showed facial nerve palsy with or without ophthalmoparesis. Temporal profile analysis of anti-glycolipid antibodies revealed that titers of anti-glycolipid IgM antibodies against GM2 and LM1 gradually decreased in patients having chronic trigeminal sensory neuropathy. In patients with acute trigeminal sensory neuropathy, elevation of anti-LM1 antibody titers continued over 12 months although anti-GalNAc-GD1a antibody disappeared. On the other hand, titers of anti-glycolipid antibodies rapidly decreased in patients with acute facial nerve palsy with or without ophthalmoparesis. We conclude that anti-glycolipid antibodies may play an important role in the development of isolated cranial neuropathy in some patients.

Chronic dysimmune neuropathy. A subclassification based upon the clinical features of 102 patients.

The Chronic Dysimmune neuropathies (CDN) are a clinically heterogeneous group of polyneuropathies united by their presumed immune mediated aetiology. At present such neuropathies are classified as Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Multifocal Motor Neuropathy (MMN) and the Neuropathies in association with serum Paraproteins (Paraproteinaemic Neuropathies). This classification fails to recognise other distinctive syndromes and is limited by heterogeneity within, and overlap between, subgroups. We have refined this clinical subclassification by a review of a consecutive series of 102 unselected patients with CDN referred to a single neurologist. We recognise 6 clinical subtypes of CDN: one sensory ataxic group; three motor-sensory subgroups (chronic motor sensory demyelinating neuropathy, subacute motor sensory demyelinating neuropathy and a multifocal motor sensory neuropathy); and two pure motor subgroups (symmetric pure motor demyelinating neuropathy and multifocal motor neuropathy). This subclassification allows distinct syndromes to be recognised and helps resolve problems of heterogeneity and overlap. Distinction between these subgroups is of immediate practical relevance to patient management. Although steroids are beneficial for most of the subgroups, this is not so for both of the pure motor syndromes which should be treated with intravenous immunoglobulin. Patients with chronic development of Motor Sensory Demyelinating Neuropathy respond less well to steroids than those with a subacute onset. An association was found between elderly patients with Subacute Motor Sensory Demyelinating Neuropathy and carcinomas. Within any clinical subgroup patients behave similarly regardless of the presence of associated paraproteins or nerve specific antibodies.

[Diagnostic approach for acquired and isolated third cranial nerve palsy: 18 case reports]. / Conduite à tenir devant une paralysie du III acquise et isolée.

PURPOSE: The aim of this work was to establish a clinical diagnostic flow chart for third nerve palsy. MATERIAL AND METHODS: [corrected] We report a series of 18 patients with third nerve palsy seen at the department of ophthalmology in the Marseille North Hospital between 1997 and 1999. All patients had a complete clinical examination and were classified into four clinic types. An etiological diagnosis was given in all cases after a systematic approach, including first intention MRI. RESULT: Three patients presented abnormal pupil reflex secondary to an aneurysm diagnosed by carotid angiography; the MRI was pathological in two cases. The 15 other patients had pupil sparing. Among them, eight patients had a total external involvement secondary to diabetes mellitus; the MRI suggested an ischelic origin in four cases (50%) showing nuclear infarctus. In seven cases the external involvement was incomplete secondary to multiple etiologies: demyelinating illness, traumatic lesions, orbital tumor, metastasis or myasthenia gravis. The MRI contributed to diagnosing four cases. CONCLUSION: The MRI must be systematically used in all the patients with isolated third nerve palsy, except for patients with pupil sparing associated with total external involvement. Ischemic etiology was the rule: simple clinical surveillance is proposed, total spontaneous regression being the norm.

The frequency of clinical variants of Guillain-Barré syndrome in Ferrara, Italy.

As the available diagnostic criteria (National Institute of Neurological and Communicative Disorders and Stroke, NINCDS) for Guillain-Barré syndrome (GBS) do not permit inclusion of clinical variants (CV) of GBS, there are few data on their occurrence and few reports of the overall incidence of the disease. A population-based study in the local health district of Ferrara, Italy in 1981-1993 selected cases fulfilling both NINCDS criteria (NINCDS GBS cases) and CV. The incidence of CV was 0.35 per 100,000 person-years (95% CI: 0.15-0.68), 0.32 when age-adjusted to the Italian population. No difference was found between CV and NINCDS GBS for male/female ratio, mean age at onset, elevated CSF protein content, seasonal pattern, or mean time delay from first neurological symptom to maximal severity. A higher frequency of antecedent infections for CV and more frequent serious disease at the nadir time for NINCDS GBS were found. A complete recovery was more frequent for CV than NINCDS GBS, but no difference was found regarding good outcome (defined by a satisfactory recovery and resumption of normal functional life). Since most findings were similar for NINCDS GBS and CV cases, they may have similar underlying pathological mechanisms. When diagnostic criteria for GBS include CV, the overall disease incidence in the Ferrara district increases from 1.87 to 2.21 cases per 100,000 person-years (the contribution of CV to the overall incidence of GBS is 15.7%). The currently available diagnostic criteria for GBS, although useful for field studies, may be too restrictive as they can entail the loss of about 15% of cases.

Inferior alveolar nerve function after mandibular osteotomies.

A total of 1034 patients who had undergone orthognathic surgery were examined after 2 years; 818 had been treated with varying types of mandibular osteotomy such as vertical ramus osteotomy, sagittal split ramus osteotomy, and genioplasty. Neurosensory function in the mental nerve region was assessed by evaluating light touch perception. The incidence of neurosensory deficiency was 216/548 (39%) after sagittal split ramus osteotomy, 26/140 (19%) after extraoral vertical ramus osteotomy, 9/78 (12%) after genioplasty and 60/650 (9%) after intraoral vertical ramus osteotomy. Additional genioplasty increased both the incidence and severity of neurosensory disturbance after intraoral vertical ramus osteotomy but did not significantly influence the neurosensory function after sagittal split ramus osteotomy. The incidences of neurosensory disturbance after mandibular osteotomies in this report correspond well with those previously reported, but the incidence of almost 40% after sagittal split ramus osteotomy must be considered a disquieting drawback of the procedure.

[Craniocervical dystonia. Pragmatic general concept or nosologic entity?]. / Kraniozervikale Dystonien. Pragmatischer Sammelbergriff oder nosologische Einheit?

The focal dystonias of cranial-nerve innervated muscles are described. They include the ocular dystonia, blepharospasmus and other facial dystonias, mandibular dystonia, pharyngeal dystonia, spasmodic dysphonia, external laryngeal dystonia, spasmodic torticollis and lingual dystonia. They share similar clinical aspects such as the inadequate co-contraction of antagonistic muscles, dystonic overflow of muscle activity to muscles not normally involved, similar facilitating and inhibitory activities and various "antagonistic gestures". Genetic, imaging, neuroanatomic, physiologic and pharmacologic findings suggest common pathogenetic mechanisms for these diseases. Similar therapeutic approaches are established. The frequent and variable combinations of these focal dystonias and their similar pathogenetic background favour their common classification as craniocervial dystonias.