Made by DATEXIS (Data Science and Text-based Information Systems) at Beuth University of Applied Sciences Berlin
Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
The prevalence of migraine and vertigo is 1.6 times higher in 200 dizziness clinic patients than in 200 age- and sex-matched controls from an orthopaedic clinic. Among the patients with unclassified or idiopathic vertigo, the prevalence of migraine was shown to be elevated. In another study, migraine patients reported 2.5 times more vertigo and also 2.5 more dizzy spells during headache-free periods than the controls.
MAV may occur at any age with a female:male ratio of between 1.5 and 5:1. Familial occurrence is not uncommon. In most patients, migraine headaches begin earlier in life than MAV with years of headache-free periods before MAV manifests.
In a diary study, the 1-month prevalence of MAV was 16%, frequency of MAV was higher and duration longer on days with headache, and MAV was a risk factor for co-morbid anxiety.
Benign paroxysmal vertigo of childhood is an uncommon neurological disorder which presents with recurrent episodes of dizziness. The presentation is usually between the ages of 2 years and 7 years of age and is characterised by short episodes of vertigo of sudden onset when the child appears distressed and unwell. The child may cling to something or someone for support. The episode lasts only minutes and resolves suddenly and completely. It is a self-limiting condition and usually resolves after about eighteen months, although many go on to experience migrainous vertigo (or vertiginous migraine) when older.
Benign paroxysmal vertigo of childhood is a migrainous phenomenon with more than 50% of those affected having a family history of migraines affecting a first-degree relative. It has no relationship to benign paroxysmal positional vertigo which is a different condition entirely.
Common triggers quoted are stress, hunger, and fatigue (these equally contribute to tension headaches). Psychological stress has been reported as a factor by 50 to 80% of people. Migraines have also been associated with post-traumatic stress disorder and abuse. Migraines are more likely to occur around menstruation. Other hormonal influences, such as menarche, oral contraceptive use, pregnancy, perimenopause, and menopause, also play a role. These hormonal influences seem to play a greater role in migraine without aura. Migraines typically do not occur during the second and third trimesters or following menopause.
Between 12 and 60% of people report foods as triggers. Evidence for such triggers, however, mostly relies on self-reports and is not rigorous enough to prove or disprove any particular triggers. A clear explanation for why food might trigger migraines is also lacking.
There does not appear to be evidence for an effect of tyramine on migraine. Likewise, while monosodium glutamate (MSG) is frequently reported, evidence does not consistently support that it is a dietary trigger.
A stroke (either ischemic or hemorrhagic) involving the posterior fossa is a cause of central vertigo. Risk factors for a stroke as a cause of vertigo include increasing age and known vascular risk factors. Presentation may more often involve headache or neck pain, additionally, those who have had multiple episodes of dizziness in the months leading up to presentation are suggestive of stroke with prodromal TIAs. The HINTS exam as well as imaging studies of the brain (CT, CT angiogram, and/or MRI) are helpful in diagnosis of posterior fossa stroke.
Vertigo is recorded as a symptom of decompression sickness in 5.3% of cases by the US Navy as reported by Powell, 2008 It including isobaric decompression sickness.
Decompression sickness can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas. This is known as isobaric counterdiffusion, and presents a problem for very deep dives. For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium, but is about 4.5 times more soluble. Switching between gas mixtures that have very different fractions of nitrogen and helium can result in "fast" tissues (those tissues that have a good blood supply) actually increasing their total inert gas loading. This is often found to provoke inner ear decompression sickness, as the ear seems particularly sensitive to this effect.
From 3% to 11% of diagnosed dizziness in neuro-otological clinics are due to Meniere's. The annual incidence rate is estimated to be about 15/100,000 and the prevalence rate is about 218/100,000, and around 15% of people with Meniere's disease are older than 65. In around 9% of cases a relative also had MD, signalling that there may be a genetic predisposition in some cases.
The odds of MD are greater for people of white ethnicity, with severe obesity, and women. Several conditions are often comorbid with MD, including arthritis, psoriasis, gastroesophageal reflux disease, irritable bowel syndrome, and migraine.
Benign paroxysmal positional vertigo - Migraine is commonly associated with BPPV, the most common vestibular disorder in patients presenting with dizziness. The two may be linked by genetic factors or by vascular damage to the labyrinth.
Ménière's disease - There is an increased prevalence of migraine in patients with Ménière's disease and migraine leads to a greater susceptibility of developing Ménière’s disease. But they can be distinguished. Ménière's disease may go on for days or even years, while migraines typically do not last longer than 24 hours.
Motion sickness is more prevalent in patients with migraine.
Psychiatric syndromes Dizziness and spinning vertigo are the second most common symptom of panic attacks, and they can also present as a symptom of major depression. Migraine is a risk factor for developing major depression and panic disorder and vice versa.
Benign paroxysmal positional vertigo (BPPV) is a disorder arising from a problem in the inner ear. Symptoms are repeated, brief periods of vertigo with movement, that is, of a spinning sensation upon changes in the position of the head. This can occur with turning in bed or changing position. Each episode of vertigo typically lasts less than one minute. Nausea is commonly associated. BPPV is one of the most common causes of vertigo.
BPPV can result from a head injury or simply occur among those who are older. A specific cause is often not found. The underlying mechanism involves a small calcified otolith moving around loose in the inner ear. It is a type of balance disorder along with labyrinthitis and Ménière's disease. Diagnosis is typically made when the Dix–Hallpike test results in nystagmus (a specific movement pattern of the eyes) and other possible causes have been ruled out. In typical cases medical imaging is not needed.
BPPV is often treated with a number of simple movements such as the Epley maneuver or Brandt–Daroff exercises. Medications may be used to help with nausea. There is tentative evidence that betahistine may help with the vertigo but its use is not generally needed. BPPV is not a serious condition. Typically it resolves in one to two weeks. It however may recur in some people.
The first medical description of the condition occurred in 1921 by Robert Barany. About 2.4% of people are affected at some point in time. Among those who live until their 80s, 10% have been affected. BPPV affects females twice as often as males. Onset is typically in the person's 50s to 70s.
Within the labyrinth of the inner ear lie collections of calcium crystals known as otoconia or otoliths. In patients with BPPV, the otoconia are dislodged from their usual position within the utricle, and migrate over time into one of the semicircular canals (the posterior canal is most commonly affected due to its anatomical position). When the head is reoriented relative to gravity, the gravity-dependent movement of the heavier otoconial debris (colloquially "ear rocks") within the affected semicircular canal causes abnormal (pathological) endolymph fluid displacement and a resultant sensation of vertigo. This more common condition is known as canalithiasis.
In rare cases, the crystals themselves can adhere to a semicircular canal cupula, rendering it heavier than the surrounding endolymph. Upon reorientation of the head relative to gravity, the cupula is weighted down by the dense particles, thereby inducing an immediate and sustained excitation of semicircular canal afferent nerves. This condition is termed cupulolithiasis.
There is evidence in the dental literature that malleting of an osteotome during closed sinus floor elevation, otherwise known as "osteotome sinus elevation" or "lift", transmits percussive and vibratory forces capable of detaching otoliths from their normal location and thereby leading to the symptoms of BPPV.
It can be triggered by any action which stimulates the posterior semi-circular canal, including:
- Looking up or down
- Preceding head injury
- Sudden head movement
- Rolling over in bed
- Tilting the head
BPPV may be made worse by any number of modifiers which may vary between individuals:
- Changes in barometric pressure — patients may feel increased symptoms up to two days before rain or snow
- Lack of sleep (required amounts of sleep may vary widely)
- Stress
An episode of BPPV may be triggered by dehydration, such as that caused by diarrhea. For this reason, it commonly occurs in post-operative patients who have diarrhea induced by post-operative antibiotics.
BPPV is one of the most common vestibular disorders in patients presenting with dizziness; migraine is implicated in idiopathic cases. Proposed mechanisms linking the two are genetic factors and vascular damage to the labyrinth.
Although BPPV can occur at any age, it is most often seen in people over the age of 60. Besides aging, there are no major risk factors known for developing BPPV, although previous episodes of trauma to the head, or inner ear infections known as labyrinthitis, may predispose individuals to future development of BPPV.
The mechanism of action of benign paroxysmal torticollis is not yet understood. It has been suggested that unilateral vestibular dysfunction or vascular disturbance in the brain stem may be responsible for the condition.
The cause of benign paroxysmal torticollis in infants is thought to be migrainous. More than 50% of infants have a family history of migraine in first degree relatives. The cause is likely to be genetic.
Although CPH is often compared to cluster headaches, it is much less prevalent, occurring in only 1–3% of those who experience cluster headaches. CPH occurs roughly in 1 in 50,000 people, while cluster headaches are comparatively more common and are found in 1 in 1000 people.
Cluster headaches occur primarily in men, while CPH is more commonly diagnosed in women. The female to male ratio of diagnosed patients can range anywhere from 1.6:1 to 2.36:1. Symptoms may begin to appear at any age, but onset usually occurs in adulthood with a mean starting age within the thirties.
Some people will report having an upper respiratory infection (common cold) or flu prior to the onset of the symptoms of vestibular neuronitis; others will have no viral symptoms prior to the vertigo attack.
Some cases of vestibular neuronitis are thought to be caused by an infection of the vestibular ganglion by the herpes simplex type 1 virus. However, the cause of this condition is not fully understood, and in fact many different viruses may be capable of infecting the vestibular nerve.
Acute localized ischemia of these structures also may be an important cause, especially in children, vestibular neuritis may be preceded by symptoms of a common cold. However, the causative mechanism remains uncertain.
This can also be brought on by pressure changes such as those experienced while flying or scuba diving.
About 20–30% of the population report to have experienced dizziness at some point in the previous year.
Labyrinthitis, also known as vestibular neuritis, is inflammation of the inner ear. It results in vertigo and also possible hearing loss or ringing in the ears. It can occur as a single attack, a series of attacks, or a persistent condition that diminishes over three to six weeks. It may be associated with nausea and vomiting. Vestibular neuronitis may also be associated with eye nystagmus.
The cause is often not clear. It may be due to a virus, but it can also arise from bacterial infection, head injury, extreme stress, an allergy, or as a reaction to medication. 30% of affected people had a common cold prior to developing the disease. Either bacterial or viral labyrinthitis can cause permanent hearing loss in rare cases. This appears to result from an imbalance of neuronal input between the left and right inner ears.
Vestibular neuritis affects approximately 35 per million people per year. It typically occurs in those between 30 and 60 years of age. There is no significant gender difference. It derives its name from the labyrinths that house the vestibular system, which senses changes in head position.
Hypnic headaches are benign primary headaches that affect the elderly, with the average age of onset being 63 ± 11 years. They are moderate, throbbing, bilateral or unilateral headaches that wake the sufferer from sleep once or multiple times a night. They typically begin a few hours after sleep begins and can last from 15–180 min. There is normally no nausea, photophobia, phonophobia or autonomic symptoms associated with the headache. They commonly occur at the same time every night possibly linking the headaches with circadian rhythm, but polysomnography has recently revealed that the onset of hypnic headaches may be associated with REM sleep.
Lithium carbonate 200–600 mg at bedtime is an effective treatment for most patients but for those that can not tolerate Lithium, Verapamil, indomethacin or methylsergilide may be tried. Two patients have also responded to flunarizine 5 mg. It has also been shown that 1–2 cups of coffee or 100–200 mg of caffeine before bed can prevent hypnic headaches.
For diagnosis of hypnic headache syndrome, headaches should occur at least 15 times per month for at least one month. Included in the differential diagnosis of a new onset nighttime headaches in the elderly is drug withdrawal, temporal arteritis, Sleep apnea, oxygen desaturated, Pheochromocytoma, intracranial causes, primary and secondary neoplasms, communicating hydrocephalus, subdural hematoma, vascular lesions, migraines, cluster headaches, chronic paroxysmal hemicrania and hypnic headache. All other causes must be ruled out before the diagnosis of hypnic headache can be made.
A ten-patient study conducted by Pareja et al. found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. Doses of the drug ranged from 25 mg per day to 150 mg per day with a median dose of 75 mg per 24-hour period.
Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued use of the drug due to adverse side effects, namely complications in the gastrointestinal tract.
According to a case study by Milanlioglu et al., 100mg of lamotrigine, an antiepileptic drug, administered twice daily alleviated all painful symptoms. No side effects were noted after two months of treatment. Dosage of lamotrigine was decreased to 50mg a day after the first two months, and no symptoms or side-effects were recorded after a three-month followup.
Use of topiramate has also been found to be an effective treatment for CPH, but cluster headache medications have been found to have little effect.
Brain related causes are less commonly associated with isolated vertigo and nystagmus but can still produce signs and symptoms, which mimic peripheral causes. Disequilibrium is often a prominent feature.
- Degenerative: age related decline in balance function
- Infectious: meningitis, encephalitis, epidural abscess, syphilis
- Circulatory: cerebral or cerebellar ischemia or hypoperfusion, stroke, lateral medullary syndrome (Wallenberg's syndrome)
- Autoimmune: Cogan syndrome
- Structural: Arnold-Chiari malformation, hydrocephalus
- Systemic: multiple sclerosis, Parkinson's disease
- Vitamin deficiency: Vitamin B12 deficiency
- CNS or posterior neoplasms, benign or malignant
- Neurological: Vertiginous epilepsy, abasia
- Other – There are a host of other causes of dizziness not related to the ear.
- Mal de debarquement is rare disorder of imbalance caused by being on board a ship. Patients suffering from this condition experience disequilibrium even when they get off the ship. Typically treatments for seasickness are ineffective for this syndrome.
- Motion sickness – a conflict between the input from the various systems involved in balance causes an unpleasant sensation. For this reason, looking out of the window of a moving car is much more pleasant than looking inside the vehicle.
- Migraine-associated vertigo
- Toxins, drugs, medications; it is also a known symptom of carbon monoxide poisoning.
Trigeminal autonomic cephalgia (TAC) is the name for a type of primary headache that occurs with pain on one side of the head in the trigeminal nerve area and symptoms in autonomic systems on the same side, such as eye watering and redness or drooping eyelids. TACs include
- Cluster headache
- Paroxysmal hemicrania (chronic or episodic)
- Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)
- Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA)
- Long-lasting autonomic symptoms with hemicrania (LASH)
TACs can be differentiated by the length and frequency of recurrence of the headaches.
Treatment for TACs varies depending on the exact type, but can include medication such as Indomethacin (in the case of chronic paroxysmal hemicrania) or acute and prophylactic therapy (in the case of cluster headache).
The cause of Ménière's disease is unclear but likely involves both genetic and environmental factors. A number of theories exist including constrictions in blood vessels, viral infections, autoimmune reactions.
Causes of dizziness related to the ear are often characterized by vertigo (spinning) and nausea. Nystagmus (flickering of the eye, related to the Vestibulo-ocular reflex [VOR]) is often seen in patients with an acute peripheral cause of dizziness.
- Benign Paroxysmal Positional Vertigo (BPPV) – The most common cause of vertigo. It is typically described as a brief, intense sensation of spinning that occurs when there are changes in the position of the head with respect to gravity. An individual may experience BPPV when rolling over to the left or right, upon getting out of bed in the morning, or when looking up for an object on a high shelf. The cause of BPPV is the presence of normal but misplaced calcium crystals called otoconia, which are normally found in the utricle and saccule (the otolith organs) and are used to sense movement. If they fall from the utricle and become loose in the semicircular canals, they can distort the sense of movement and cause a mismatch between actual head movement and the information sent to the brain by the inner ear, causing a spinning sensation.
- Labyrinthitis - An inner ear infection or inflammation causing both dizziness (vertigo) and hearing loss.
- Vestibular neuronitis - an infection of the vestibular nerve, generally viral, causing vertigo
- Cochlear Neuronitis – an infection of the Cochlear nerve, generally viral, causing sudden deafness but no vertigo
- Trauma – Injury to the skull may cause either a fracture or a concussion to the organ of balance. In either case an acute head injury will often result in dizziness and a sudden loss of vestibular function.
- Surgical trauma to the lateral semicircular canal (LSC) is a rare complication which does not always result in cochlear damage. Vestibular symptoms are pronounced. Dizziness and instability usually persist for several months and sometimes for a year or more.
- Ménière's disease - an inner ear fluid balance disorder that causes lasting episodes of vertigo, fluctuating hearing loss, tinnitus (a ringing or roaring in the ears), and the sensation of fullness in the ear. The cause of Ménière's disease is unknown.
- Perilymph fistula – a leakage of inner ear fluid from the inner ear. It can occur after head injury, surgery, physical exertion or without a known cause.
- Superior canal dehiscence syndrome – a balance and hearing disorder caused by a gap in the temporal bone, leading to the dysfunction of the superior canal.
- Bilateral vestibulopathy – a condition involving loss of inner ear balance function in both ears. This may be caused by certain antibiotics, anti-cancer, and other drugs or by chemicals such as solvents, heavy metals, etc., which are ototoxic; or by diseases such as syphilis or autoimmune disease; or other causes. In addition, the function of the semicircular canal can be temporarily affected by a number of medications or combinations of medications.
Many conditions cause dizziness because multiple parts of the body are required for maintaining balance including the inner ear, eyes, muscles, skeleton, and the nervous system.
Common physiological causes of dizziness include:
- inadequate blood supply to the brain due to:
- a sudden fall in blood pressure
- heart problems or artery blockages
- loss or distortion of vision or visual cues
- disorders of the inner ear
- distortion of brain/nervous function by medications such as anticonvulsants and sedatives
- result of side effect from prescription drugs, including proton-pump inhibitor drugs (PPIs) and Coumadin (warfarin) causing dizziness/fainting
The cause of AHC is unknown. It was initially thought to be a form of complicated migraine because of strong family histories of migraine reported in AHC cases. AHC has also been considered to be a movement disorder or a form of epilepsy. Suggested causes have included channelopathy, mitochondrial dysfunction, and cerebrovascular dysfunction. The disorder most closely related to AHC is familial hemiplegic migraine, and this was recently discovered to be caused by a mutation in a gene for calcium channel receptors. It is suspected that AHC may be caused by a similar channelopathy, and this is a current area of investigation into the cause of AHC. An association with "ATP1A2" mutation has been found in some patients, but other studies have found no mutations and thus a lack of evidence that mutations which cause AHC are in the same genes as mutations which cause familial hemiplegic migraine.
Because alternating hemiplegia of childhood is so rare, there is no increased risk of AHC for the children of siblings of someone with AHC, but it is believed to be autosomal dominant, by which a person with AHC has a 50% change of passing the disorder on to their children. AHC is questionably a progressive disease, because cognitive abilities do appear to decline over time. This cannot be completely determined however, because the mechanism of AHC's progression is unknown. It is likely that it is caused by a generalized cellular dysfunction caused by a mitochondrial disorder. However, studies involving mechanisms of AHC have been inconclusive. Experts currently researching this disorder believe that the cause of AHC is a mutated ion channel. This would make the cause difficult to find because one disrupted channel may be represented differently in different tissues. This mutation is suspected because the most closely related disease, FHM, is also caused by a mutated ion channel. A small number of genes which were suspected to carry a mutation for AHC have been screened for sodium channel protein mutations, ATP pump mutations, and excitatory amino acid transmitter mutations. None of these have yet been successful in determining the underlying cause of AHC.
One large study has identified the gene ATP1A3 as the likely genetic cause of this disorder. This gene is located on the long arm of chromosome 19 (19q13.31).
THS is uncommon in both the United States and internationally. In New Zealand, there is only one recorded case, there is also one recorded case in New South Wales, Australia. Both genders, male and female, are affected equally, and it typically occurs around the age of 60.