Paroxysmal Vertigo Research Articles

Effects of ROIN® (Cinnarizine) on Vertigo

Cinnarizine was administered to a total of 35 patients with vertigo, and the therapeutic effects were reviewed. As a result of efficacy-judgement of the whole improvement rate on subjective and objective findings, effectiveness of this drug was observed for the treatment of Meniere's disease, “forme fruste” Meniere's disease, benign paroxysmal cephalic vertigo, and spondylocerebro-basal arteriocirculatory insufficiency. Moreover, the effect was observed on concomitant symptoms such as nausea, vomiting, heavy feeling of the head, and headache. The effect on tinnitus was minor, and no effect was observed in cases of “hard of hearing”. As for the side effects, one patient complained of somnolence.

An experimental evidence of etiology in postural vertigo.

The symptoms and findings of postural vertigo vary, so the causation of this disturbing unpleasantness is obviously not always the same. The effect of minute changes of the gravitational force upon the otolith organs was suspected. Disturbances of circulation in the head and neck subsequent to postural changes were implicated. Abnormalities in the ‘neck reflexes’ was another consideration. Small, circumscribed lesions produced in the cerebellum created typical postural nystagmus in the experimental animal. More recently, an unexplained histologic change of otolith detachment was believed evoking the symptoms. The clinical entity, termed as the benign paroxysmal postural vertigo, was identified with most of the above-mentioned etiological factors. Observations made on the many hundreds or thousands of patients on the indeed benign and self-limiting nature of this condition tended to rule out circulatory, central nervous or otolithic etiologies. Instead, because certain neck movements appear to trigger the symptoms, the possibility of a neural rather than a vascular causative factor was examined in animal experimentation. It could be established that mechanical stimulation of the neural plexus, or the sympathetic cervical nerve, in the dog will excite the ipsilateral vestibular end organs with a short burst of impulses. The experimentally evoked reflex activity fatigues but it is reproducible. These observations are applicable in explaining the pathomechanism of the benign type paroxysmal postural vertigo. Postural vertigo of inner ear or CNS origin should be differentiated from similar, positioning symptoms where no specific cause was detectable. This idiopathic condition is a response of the neural, sympathetic plexus on the exposed surface of the vertebral artery. For better identification of this common disease, in contrast to benign paroxysmal postural vertigo (BPPV), positioning neurocervical vertigo (PNV) is suggested.

Vestibular dysfunction associated with benign paroxysmal vertigo

Benign paroxysmal vertigo (BPV) is a clinical syndrome of vestibular origin although generally no evidence of vestibular dysfunction can be demonstrated with conventional tests. In a review of 1350 consecutive dizzy patients, there were 125 with BPV and of these, 33 underwent a quantitative rotational test of vestibular function. The rotational results showed reduces vestibular system gain for these BPV patients. In addition, they could be subdivided on the basis of a normal or shorter cupular time constant (Tc). Separation of patients into diagnostic categories revealed that those categorized as cupulolithiasis and viral labyrinthitis had a normal Tc range and those categorized as trauma and idiopathic had a short Tc. The reduced gain and short Tc in the latter group suggest hair cell and/or nerve damage since these same changes occur in patients with destructive peripheral vestibular disease.

Benign paroxysmal vertigo of childhood.

Thirty-three cases of benign paroxysmal vertigo in childhood have been seen at our institution since the disorder was recognized ten years ago. Progression from paroxysmal torticollis of infancy to paroxysmal vertigo of childhood is documented. Ear infections and allergy appeared causative in a few, but not most, of the cases. The most important consideration for the pediatrician is to rule out epilepsy and brain tumor. Parents should be reassured that the condition is benign, and that the attacks will cease in a few months or years.

Advanced Meniere's disease. A study of 356 severely disabled patients.

A selected material of 356 patients with Meniere's disease, all severely disabled by paroxysmal vertigo, was analysed. The question under study was to what extent and in what way the severe vertigo is reflected in the caloric reaction and in the level of hearing. The caloric response, expressed as differences in right/left sensitivity, was reduced in 59% and exaggerated in 1% of the patients; in the remaining 40% it was normal. The median values for pure tone audiogram, speech reception threshold and speech discrimination score were 56 dB,60 dB and 54%, respectively. The hearing deteriorated considerably in the early stage of the disease, but the hearing level stabilised with time. A parallelism between acoustic and vestibular dysfunction was demonstrated. Reduction of the pure tone threshold was accompanied by a progressive decrease in caloric response. The frequency of bilateral cases increased with lengthening duration of illness. All patients included in this investigation have since undergone operation.

Paroxysmal dyseguilibrium in the migraine syndrome of childhood.

Paroxysmal dysequilibrium, common in children, is often a symptom of the migraine syndrome of childhood. In some patients with classical migraine, the vertigo is due to ischemia within the basilar artery distribution, but in others, the site of the cerebral ischemia cannot be accurately defined. Cases of vertigo unassociated with headache that resemble those described by Basser (1964) as benign paroxysmal vertigo of childhood are also described. Follow-up studies of these patients whose symptom was originally diagnosed as a migraine equivalent indicate that 50% subsequently developed classical migraine.

More drugs for meniere’s disease

Ménière’s syndrome is paroxysmal vertigo with tinnitus and sensorineural (perceptive) hearing loss. The hearing loss may be slowly progressive, fluctuating or sudden. Where no organic cause can be discovered the condition is called Ménière’s disease. The syndrome is found in patients with bone disease involving the otic capsule such as otosclerosis, osteitis deformans or late syphilis. It may also follow labyrinthine trauma or be associated with a wide variety of diseases interfering with the blood supply to the brainstem or inner ear. Endolymphatic hydrops has been demonstrated in all these conditions, and it is believed that it may occur also in Ménière’s disease. Other causes of the syndrome include inflammatory or demyelinating disorders or tumours involving the eighth nerve. Many drugs have been used to treat Ménière’s disease, but with little success. Drugs investigated in recent years include cinnarizine (an antihistamine which has been used for vertigo and motion sickness), betahistine (an orally active histamine analogue) and hydrochlorothiazide.

Benign paroxysmal vertigo of childhood

SUMMARYSeventeen children with benign paroxysmal vertigo have been described. The clinical features consist of the onset of recurrent, very brief attacks of vertigo in a child less than 3 years old, with full preservation of awareness and speech during each attack and a tendency to spontaneous disappearance of attacks over a period of several months to several years. The results of vestibular function tests in the subjects and in 14 control children of the same age group are presented and discussed. The narrow range of normal variation and the ease with which the diagnosis of BPV can be confirmed by the use of Hallpike caloric tests are emphasized. The differential diagnosis of BPV and similar paroxysmal disorders is reviewed. Our impression of the favorable results of treatment with dimenhydrinate in children having frequent attacks is recorded.

Diabetes insipidus

Dr. Philip Lebovitz, Junior Assistant Resident in Medicine, Jewish Hospital of St. Louis and Assistant in Medicine, Washington University School of Medicine: A 62-year-old white man was hospitalized on March 27, 1968, because of increasing exertional dyspnea of two weeks' duration. Thirty years previously a diagnosis of rheumatic heart disease with atrial fibrillation had been made. In 1953, following a pulmonary embolus, the patient was treated with warfarin sodium for several months. In 1956 the patient was given digoxin and in 1964 chlorothiazide. Three months before hospitalization furosemide was substituted for chlorothiazide. One month later the patient noticed increasing thirst, a craving for ice water, polyuria, and nocturia. There was no chest pain, cough, hemoptysis, syncope, orthopnea, paroxysmal nocturnal dyspnea, headache, vertigo, or visual disturbance. A stone in the left kidney was removed surgically 12 years before admission and nine years later a suprapubic prostatectomy was performed. Physical examination revealed

Familial leukemia and osteogenesis imperfecta

Migraine is a hereditary disorder affecting the stability of the cerebral circulation. The attacks are recurrent and divided into a vasoconstrictive and vasodilatative phase. During the vasoconstrictive phase, cerebral ischemia occurs in the distribution of either the carotid or the basilar systems. The vasodilatative phase is characterized by headache and vomiting. The severity and consequently the symptomatology associated with each phase of the migraine varies from individual to individual and from attack to attack. Vasoconstriction is typically characterized by ischemia in the distribution of the carotid system. Less frequently, the basilar system is involved, as manifest by vertigo and ataxia? In early childhood, the headache phase is less apt to develop or be recognized, and the episodes consist mainly of the vasoconstrictive symptoms and the final period of somnolence? The proband of this report first presented at age two with symptoms of paroxysmal vertigo. The attacks insidiously changed in character from isolated vertigo to fairly typical migraine. Symptoms of benign paroxysmal vertigo developed in a younger brother who is now two years old. Family history reveals a high incidence for migraine in the maternal line. The suggestion is therefore made that paroxysmal vertigo of childhood may at times be an early manifestation of migraine rather than a form of vestibular neuronitis.

Migraine as a cause of benign paroxysmal vertigo of childhood

T ~ E S Y N D R O Z a E OF paroxysmal vert igo of chi was described in 1964 as a var ie ty of ves t ibular neuronitis. 1 In essence the d isorder is character ized by paroxysms of ver t igo as an almost isolated symptom dur ing the first three or four years of life. The at tacks are of sudden onset and grea t severity, bu t brief in durat ion. Nystagmus and pal lor are common, while vomit ing is less often associated. T h e child is l imp dur ing the episode bu t suffers no loss of consciousness or headache. At tacks recur for six months to a year and then cease spontaneously. L a b o r a t o r y studies are not contr ibutory wi th the except ion of caloric testing, which general ly demonst ra tes a mild to moderate canal paresis. The roentgenograms of the skull and the e lec t roencephalogram are character is t ica l ly normal . This pape r reports two siblings who display the syndrome of benign paroxysmal vert igo and in whom the attacks progressively conver ted into classical migraine. The relat ionship between recurrent vert igo and migraine in chi ldhood is considered.

STUDIES ON THE CORRELATION BETWEEN THYROID FUNCTION AND Ménière's SYNDROME

The author investigated clinically the correlation between thyroid function and Ménière's syndrome.The results are, on the whole, as follows: 1) As the results of thyroid function tests such as serum protein-bound-iodine(P.B.I.), radioactive iodine(I131) uptake of the thyroid gland(24 hour method), basal metabolic rate(B.M.R.), blood cholesterol, and the enlargement of the thyroid gland on 50 cases of Ménière's syndrome(Typical 25 cases and atypical 25 cases), the hypofunction of the thyroid gland was seen in 52% of typical cases and 44% of atypical cases. 2) The typical 25 cases of Ménière's syndrome have shown a tendency that many patients in the hypofunction group of the thyroid gland, had generally shown slender type, allergic constitution, hypotension, instability of autonomic nervous system, and anaemia;also, u tendency that many of them have shown CP at the time of caloric test or the slight tendency of reversibility of paroxysmal vertigo. 3) Between the group of hypothyroidism and normal group, no difference of thyroid function was found through the duration of sickness(the duration from the beginning of sickness to the time of clinical function test).In general, a tendency has been seen that the thyroid function had declined slightly in the period of parexysm rather than in the quiet period. 4) After giving proper doses of thyradin for 12 cases among the hypothyroid group of Menere's syndrome, the author recognized the effective rate of 66.6% for vertigo, 36.4% for tinnitas, 33.3% for hard of hearing, 66.7% for headache, or heavy feeling in the head, 62.5% for shoulder stiffness, and 71.4% for general languor respectively. 5) As a result of vestibular function test and hearing test on 10 cases of primary myxedema, which is the typical hypothyroid sickness, only slight disorder of vestibular function and hearing ability in half the number was seen.There was no case which could be diagnosed as the typical Ménière's syndrome. 6) According to the results of T.S.H.test carried out on 9 cases of the hypothyroid group of Ménière's syndrome, the author came to the conclusion that the lowering of the thyroid function might be secondary caused mainly by factor of hypophysis. The abovementiond results show that the thyroid function is always closely related with the complicated clinical picture of this syndrome as a general, background factor.In order to understand various clinical pictures of Ménière's syndrome, the author asserts that it might furnish much information in investigations of functions of various endocrine glands including the thyroid function. It seems clinically significant that the medical treatment of this syndrome, which hitherto has been apt to be focalised only to the local symptomatic therapy, should be done from the general point of view.

Paroxysmal vertigo with nystagmus and parotid swelling in a patient suffering from unilateral total deafness following concusion.

It is well known that severe head injury may give rise to pronounced disturbances of acoustic-vestibular function which may even become extinguished if the labyrinth is involved by a fracture of the temporal bone. Less attention has been given to the fact that severe acoustic-vestibular disturbances may be observed also after less severe head injuries. This is exemplified by the present patient who also had recurrent parotid swelling. <h3>Report of a Case</h3> The patient was a boy, aged 11 years, the second of a family of 3. The pregnancy had been uneventful apart from minor vaginal bleeding in the 3rd month. Delivery occurred at term and was normal; birth weight 4,700 gm. The boy was fit and thrived normally during infancy. At the age of 2½ years he fell head first, into a basement passage, from the ground floor down 5 or 6 stone steps. He was brought to a

The factor of heredity in labyrinthine deafness and paroxysmal vertigo; Ménière's syndrome.

The factor of heredity in labyrinthine deafness and paroxysmal vertigo; Ménière's syndrome.

CHICAGO LARYNGOLOGICAL AND OTOLOGICAL SOCIETY

<h3>A SYMPOSIUM ON MÉNIÈRE'S SYMPTOM COMPLEX</h3><h3>Otolaryngologic Point of View. Presented by Dr. John R. Lindsay.</h3> The term "Ménière's syndrome" has been used in connection with a group of diseases with paroxysmal vertigo, tinnitus and deafness which could not be explained on the basis of inflammatory disease, tumor or trauma. Clinical and pathologic observations have more recently made it possible to distinguish several entities within this general group. The term "Ménière's disease" has recently been used to denote a clearcut clinical syndrome of recurrent attacks of vertigo, tinnitus and deafness. It is fairly well established that in the patients with this disease the pathologic condition in the inner ear is labyrinthine hydrops. The term "pseudo Ménière's disease" has been used to denote attacks of vertigo without auditory symptoms and without other neurologic signs. This clinical picture is comparatively common and serves to complicate the diagnostic problem. The questions the otologist

MÉNIÈRE'S SYNDROME

From the large group of cases in which vertigo is a complaint may be isolated a group of cases in which the course of the disorder is a chronic one and in which intermittent paroxysmal vertigo occurs in association with nausea, vomiting, loss of hearing and tinnitus on the side of the affected ear, occasionally with nystagmus, but without anatomic or pathologic changes which identify the disease. MEDICAL TREATMENT Previous to the paper of Furstenberg, Lashmet and Lathrop 2 in 1934, in which favorable results were reported to have been obtained in fourteen cases of typical Meniere's syndrome in which treatment with a diet low in sodium and with ammonium chloride was instituted, cases of this nature had been variously dealt with at the Mayo Clinic. From the files of the Mayo Clinic the histories of patients considered to present clinical evidence of the typical Meniere's syndrome were selected, comprising