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2 What’s Bugging You? Alliaceous Therapy for Ekbom Syndrome
- Fizah S. Chaudhary, Jasir T. Nayati, Ather M. Ali, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 24 / Issue 1 / February 2019
- Published online by Cambridge University Press:
- 12 March 2019, pp. 175-176
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Study Objective
Delusional parasitosis, or Ekbom syndrome, is a fixed false belief of being infested by parasites [Bellanger 2009]. With easy accessibility of the internet, serving as a vital tool in acquiring myriad information, these delusions typically arise and can be fueled by external sources as self-research [Bell2005]. For instance, garlic (allium sativum) has been reported to exhibit anthelmintic activity against cestodes (tapeworms), proving to be a natural treatmentoption [Abdel-Ghaffar 2010]. Without proper instructions, guidelines, or control of such information, psychopathological manifestations may be derived.
MethodsA young adult male presented with severe psychosis. He reports responding to an internal stimuli, non-command auditory hallucinations, and paranoid ideations specifically in regards to his body and health for several weeks. Prior to presentation, he experienced abdominal pain and constipation for five days, but attributed it to the belief of having tapeworms. He stated that he researched cures for several days using the internet and found garlic as a treatment option. He attempted to alleviate his symptoms by ingested 197 pills of 1,000 milligram (mg) garlic supplements, two 100mg bisacodyl laxatives, and five 100mg docusate stool softeners in one day. He denies any suicidal/homicidal ideations, illicit substance abuse, deja-vu, and jamais-vu.
ResultsPsychiatric examination is as follows: Mental Status Examination: awake, alert, and oriented x3. General Appearance: disheveled. Speech: soft, mumbling, and minimally non-responsive. Psychomotor Activity: moderately sedated. Eye Contact: poor. Mood: dysphoric. Affect: flat. Thought Process: flight of ideas. Thought Content: preoccupied. Judgement/Insight: poor. Immediate/Recent Recall: poor. Remote Memory: poor.
ConclusionDelusional parasitosis and somatic parasitic infestation has dire consequences in which one's health can become compromised. For those suffering from parasitosis, addition of garlic in food as well as garlic supplements of 50mg/kg body weight has been reported as a possible naturopathic treatment option in Cryptosporidiosis and Schistosoma mansoni [Gaafar 2012; Nahed 2009]. In addition, it was found that a dose of 1.2mg for three days was efficient, safe, and shortens the duration of treatment for parasites [Soffar 1991]. However, this patient ingested 197,000mg of garlic supplements without experiencing symptoms of overdose. This may include burning sensation of the mouth or stomach, flatulence, nausea/vomiting, diarrhea, thrombocytopenia, and anaphylaxis [Bayan 2014]. The efficacy of garlic for treatment of true parasitosis is unknown, but can be found in common practice especially those who practice naturopathic medicine. In this case, it is unlikely to have a positive effect, especially when delusional in nature. The use of homeopathic medication in those with true parasitosis and delusional parasitosis should be queried.
Funding Acknowledgements: Smell & Taste Treatment and Research Foundation
24 CerefolinNAC Therapy-Induced Dysgeusia
- Jasir T. Nayati, Fizah S. Chaudhry, Tajinder Parhar, Ather M. Ali, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 24 / Issue 1 / February 2019
- Published online by Cambridge University Press:
- 12 March 2019, p. 186
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Introduction
CerefolinNAC (CFLN-NAC) is a prescription medical food reported to help with mild to moderate cognitive impairment [Pamlab 2017]. It contains L-methylfolate calcium (6mg), methylcobalamin (2mg), Schizochytrium (90.3mg), and N-acetylcysteine (NAC) (600mg) [Pamlab 2017]. However, dysgeusia secondary to CFLN-NAC therapy has not heretofore been described.
MethodsA 64 year-old female presented with an eight year history of progressively decreased ability to smell and taste of unknown origin. CFLN-NAC was prescribed off-label to treat her hypogeusia and hyposmia. Three days after treatment initiation, her taste sensations gradually returned and she was able to describe food as bitter, salty, sour and sweet. Also, she was able to decipher the taste of different nuts, such as almonds, macadamia, pecans, and peanuts at baseline. However, her taste sensations became distorted and she was unable to distinguish specific foods. She reported that most food tasted bland, but she was still able to sense textures of various foods describing them as, “crunchy, but without taste.” She denied any oral pain, xerostomia, hot flashes, and psychological distress. CFLN-NAC was continued for three months and her hypogeusia improved from 20% to 80%. Her dysgeusia persisted, but remitted once CFLN-NAC was discontinued.
ResultsAbnormalities in physical examination: General: scalloped tongue, decreased blink frequency, and hypokinesia. Cranial Nerve (CN) Examination: Olfaction (CN I) Testing: Alcohol Sniff Test: 8 (hyposmia). Pocket Smell Test: 2 (hyposmia). Olfactometer Identification Test: Left: 5 (anosmia); Right: 12 (hyposmia). CN III, IV, VI: saccadization on horizontal eye movement. Motor Examination: hypokinetic movements and 1+ cogwheel rigidity in bilateral upper extremities. Drift Test: bilateral abductor digiti minimi signs with cerebellar spooning. Reflexes: absent patellar and Achilles bilaterally. Hoffman’s Reflex: present bilaterally. Other: Magnetic resonance imaging (MRI) of the brain with contrast was unremarkable.
ConclusionWhen treating taste impairments, vitamins and minerals have been found to enhance the effect of non-injured nerves, but they do not repair damaged nerves. The presence of a scalloped tongue may suggest nerve injury of unknown proportion, and can either diminish or alter taste. CFLN-NAC may have enhanced the gustatory stimulus of the non-injured nerves. This transient increase could have either caused her dysgeusia or possibly unmasked the dysgeusia secondary to a scalloped tongue. Notable impairments found in her exam evince Parkinson’s disease as a possible etiology, but structural abnormalities were not seen on brain MRI, making this unlikely. Conversely, the relatively rapid resolution after terminating CFLN-NAC strongly suggests that this is not merely a coincidence, but rather an origin. Those initiated on CFLN-NAC should be queried for new onset of dysgeusia and warrant other treatment options.
Funding Acknowledgements: Smell & Taste Treatment and Research Foundation
25 Ventriculoperitoneal Shunt as a Meteorologist: Medtronics Shunt Headaches Vaticinating Climatic Perturbation
- Jasir T. Nayati, Syed Mohyuddin, Tajinder Parhar, Ather M. Ali, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 24 / Issue 1 / February 2019
- Published online by Cambridge University Press:
- 12 March 2019, pp. 186-187
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Introduction
Neurological conditions can be influenced by meteorological parameters. Some may predict weather changes, such as migraines [Marrelli 1988], burning mouth syndrome [Hirsch 2017], phantosmia [Hirsch 2013], and Bell’s Palsy [Danielides 2001]. However, climatic conditions inducing headaches in those with ventriculoperitoneal shunt (VPS) placements have not heretofore been described.
MethodsA 46-year-old female presented with epochs of headaches coinciding with climatic changes. She had hydrocephalus secondary to infantile meningitis that was treated with a Medtronics Strata II adjustable VPS. After multiple revisions, she noticed a headache occurring only before thunderstorms or snowstorms. These headaches were constant, bilateral, “halo-like” downward pressure located only around her parietal regions. It persists all day and does not dissipate after onset, regardless of the storm passing. She rates it 8/10 on the pain scale, and is exacerbated by jarring, sneezing, and bending forward. It is only alleviated with acetazolamide, diminishing to 0/10. She denies any pain relief when supine, pain radiation, rhinorrhea, auras, or correlating psychological distress.
ResultsAbnormalities in physical examination: General: hammer toes. Neurological Examination: Cranial Nerve (CN) Examination: CN III, IV, VI: saccadization on horizontal eye movement and bilateral ptosis (left > right). CN IX, X: right uvula deviation. Motor Examination: left upward-outward drift with a positive left abductor digiti minimi sign. Reflexes: 3+ bilateral biceps, brachioradialis, and patellar; 3+ right tricep and 4+ left tricep. Hoffman's Reflex: positive bilaterally (left > right). Neuropsychological Tests: Mental Status Examination: Recent Recall: 1/4 objects in three minutes without improvement with reinforcement. Go-No-Go Test: 6/6. Animal Fluency Test: 21 (normal). Center for Neurologic Study-Lability Scale: 23 (pseudobulbar affect).
ConclusionHow climatic changes induce VPS headaches remains unclear. Barometric changes have been reported to cause sinus engorgement [Kaliner 2009], somatic pain [Silove 2006] and can worsen anxiety and depression [Delyukov 1999]. Meteorological parameters may have induced or exacerbated her depression and anxiety, amplifying pain perception. Alternatively, barometric pressure can cause an increase in other somatic pains and stresses, which can augment awareness of additional, unrecognized somatic pains. It is also possible for barometric pressure to cause pain via nasal sinus or mucosal engorgement; thus, mimicking her VPS headache. Lastly, however unlikely, her pain may be a result of a transient VPS malfunction. The mechanism for such can be attributed to transient pressure changes caused by fluctuating blood pressure, inducing brief intrinsic intraperitoneal pressure changes. Nevertheless, querying patients suffering from VPS headacheswhether climatic changes play a role in their symptoms is warranted.
Funding Acknowledgements: Smell & Taste Treatment and Research Foundation
137 Menstrual Synchrony of Burning Mouth Syndrome
- Jasir T. Nayati, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 23 / Issue 1 / February 2018
- Published online by Cambridge University Press:
- 15 June 2018, p. 86
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Study Objective
Burning mouth syndrome (BMS) is characterized by oral mucosal burning sensations, with normal clinical and laboratory results. Menstrual synchrony of migraines and epilepsy have been discussed; however, menstrual synchrony of BMS has not heretofore been described.
MethodsCase Study: A 29 year old right-handed female exhibited intermittent BMS symptoms, one month after suffering a left parietal infarction. She describes the pain as a burningsensation, localized to the bilateral and anterior aspects of her tongue. It lasts for four days, starts three days prior to her menses, and occurs twice a month. She is unable to correlate any patterns or triggers that may cause to exacerbate her BMS. She denies any taste disturbances, hot-flashes, night sweats, and perspiration.
ResultsAbnormalities during neurological examination were noted. Cranial nerves (CN) III, IV, and VI showed bilateral lateral first degree end-gaze unsustained nystagmus. CN IX and X showed decreased bilateral gag reflex. A right pronator drift with a right abductor digiti minimi sign was seen in the motor examination. The cerebellar examination was positive for bilateral dysmetria during the Finger-To-Nose examination, and exhibited Holmes rebound phenomena, right more than left. Sensory examination showed decreased light touch in the lower extremities, right more than left. Hoffman reflex was bilaterally positive. Mental status examinations demonstrated poor similarity interpretation and calculation ability. Her neuropsychiatric testing was normal, and included the Go-No-Go and Animal Fluency Testing. MRI of the brain exhibited gliosis/laminar necrosis in the left inferior parietal lobe, and an 8mm descent of cerebellar tonsils below the foramen magnum.
ConclusionThe potential mechanism for catamenial BMS is manyfold. Estrogen and progesterone both have nociceptive properties. Premenstrual drop or reduction of estrogen and progesterone may act to disinhibit pain [Vincent 2008], with pain modulation being more effective during the ovulatory phase (high estrogen and low progesterone) [Rezaii 2012]. Depression in the presence of Late Luteal Phase Dysphoric Disorder may function to exacerbate the perception of underlying pain throughout the body, including the mouth and tongue. Decrease in estrogen and progesterone levels may also alter salivary output and composition. This may allow baseline reduction of proprioceptive input on the tongue, thus acting through Melzack and Wall’s Gate Control Theory of Pain to disinhibit small C fibers, which is perceived as burning pain [Melzack 1978]. Along with menses, olfactory ability drops, and food preferences are often reported to change [Keller 2013]. A decrease in estrogen and progesterone can also enhance trigeminal nerve sensitivity [Martin 2007], which exacerbates pain. This may indirectly influence or be associated with her BMS. Such observations justifies a trial of hormonal agents for therapy of BMS.
Funding AcknowledgementsSmell and Taste Treatment and Research Foundation
119 Refraction Focus Hallucination: The Role of Increased Excitation at Thalamus in Complex Visual Hallucination
- Chunhui Yang, Jasir T. Nayati, Khurram Janjua, Asma Ahmed, Angela Rekhi, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 23 / Issue 1 / February 2018
- Published online by Cambridge University Press:
- 15 June 2018, pp. 75-76
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Study Objective(s)
The pathogenesis of complex visual hallucination in patients without visual lesions, appearing with eyes open and resolving with eyes closed, has been described to be associated with increased excitation at the lateral geniculate nucleus (LGN) and pulvinar of the thalamus (Winton-Brown, 2016). This reduces thefidelity of retinogeniculate transmissions and enhances aberrant projections to the visual cortex. Loss of the central sensory filtering function of the pulvinar increases “signal to noise ratio” in visual transmission. While visual hallucinations have been reported to disappear on eye closure (Manford, 1998), visual aberration with correction with refractionfollowed by focusing on actual visual images and visual hallucinations has not heretofore been reported. Such a case is presented.
MethodCase study: This 28-year-old, myopic, right-handed man, at 5 years of age began hallucinating vivid images of people. The visual hallucinations were triggered only with his eye open. He was myopic and without visual correction, his visual sphere would be blurred. The visual hallucinations were also blurred without visual correction. With refraction, the hallucinations became clearly in focus. He would close his eyes and the visual hallucinations disappeared but would reappear in the same position upon opening his eyes. For over 20 years, he experienced about 100 hallucinations a day. Electroencephalography (EEG) revealed continuous spikes and slow waves in bilateral temporal lobes, consistent with temporal lobe status epilepticus. After treatment with diphenylhydantoin the frequency and duration of the hallucinations markedly decreased to a second epoch every other day. However, the characteristic of the hallucinations remained the same (people).
ResultsThis phenomenon may involve epilepsy induced excitation of the thalamus. This then acts to reduce the fidelity of retinogeniculate transmission and increase “signal to noise ratio” in visual transmission. This may contribute to complex visual hallucinations with eyes open. The hallucinated figures becoming clearer with eyeglasses provides support that this complex hallucination arises in the pathway from retina-LGN-cortex, not from stored visual associated cortex of top-down cortical release.
ConclusionsGiven the above, those with visual hallucinations should be queried as to the influence of refraction on the clarity of hallucination.
FundingNo funding.
139 Burning Mouth Syndrome After Hemicolectomy and Hyperalimentation
- Jasmine M. Campbell, Jasir T. Nayati, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 23 / Issue 1 / February 2018
- Published online by Cambridge University Press:
- 15 June 2018, pp. 87-88
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Study Objective
Burning mouth syndrome (BMS) is characterized by a burning sensation in the tongue or other oral sites [Grushka 2002]. Vitamin B complex deficiencies have been associated with BMS, including B1 (thiamine) [Lamey 1988]. Replacement with thiamine and other B vitamins was noted to cause relief of BMS in 34 of 150 patients [Lamey 1988]. BMS secondary to vitamin deficiencies have been discussed; however, hemicolectomy and hyperalimentation associated thiamine deficiency inducing chronic BMS has not heretofore been described.
MethodsCase Study: A 63 year old female presents with a two year history of BMS pain, two weeks following a hemicolectomy from terminal ileum to transverse colon and five days of hyperalimentation. She describes it as a burning pain, 8/10 in severity, localized to both lips, anterior tongue, and middle tongue. It is aggravated with eating and drinking, increasing to 10/10 on the pain scale. Alleviation of pain is seen when ice, Blistex, or lidocaine-mouthwash is used, decreasing the pain to 4/10. Diurnal variation was noted, wherein the pain is exacerbated later in the evening.
ResultsAbnormalities in neurological examination: Motor Examination: abductor pollicis brevis 4/5 bilaterally. Drift testing with bilateral cerebellar spooning and bilateral abductor digiti minimi signs. Cerebellar Examination: rapid alternating movements are decreased in the left upper extremity. Reflex Examination: Deep Tendon Reflexes: Brachioradialis: 3+ bilaterally. Biceps: 3+ bilaterally. Triceps: 3+ bilaterally. Ankle Jerk: 2+ bilaterally with delayed return. Hoffman reflex: positive bilaterally. Serum Thiamine level: 66 nmol/L (normal 70-180 nmol/L).
ConclusionAlthough, BMS can be seen with thiamine deficiency [Lamey 1988], it has yet to be described status-post hemicolectomy and hyperalimentation. Thiamine is absorbed systemically in the upper jejunum, as well as in duodenum and ileum in conjunction with folate [Friedamann 1948]. Thiamine deficiency is associated with Wernicke-Korsakoff Syndrome and Wet/Dry Beri-Beri; however, these abnormalities are associated with a significant decrease of serum vitamin B1 [Martin 2004]. Even with near normal levels of thiamine, her BMS pain may be a prodromal syndrome which may act as a biological marker of dietary vitamin deficiency.
BMS is highly prevalent in postmenopausal women, wherein trigeminal nerve sensitivity may amplify and worsen pain, given a decrease in estrogen and progesterone [Martin 2007], indirectly influencing her BMS pain. Salivary output and composition can alter due to a drop in estrogen and progesterone as well, allowing baseline reduction of proprioceptive input on the tongue. Ergo, acting through Melzack and Wall’s Gate Control Theory of Pain to disinhibit small C-fibers, it may be perceived as burning pain [Melzack 1965]. Given this case, in those who undergo abdominal surgery or hyperalimentation, query regarding BMS symptoms is warranted.
Funding AcknowledgementsSmell and Taste Treatment Research Foundation
138 Gait Ignition Failure Syndrome Secondary to Spinal Stenosis
- Jasir T. Nayati, Angela Rekhi, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 23 / Issue 1 / February 2018
- Published online by Cambridge University Press:
- 15 June 2018, pp. 86-87
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Case Objective
Gait ignition failure syndrome, where immobility occurs only upon initiation of ambulation and normal gait ensues once entrained, has been reported with frontal lobe and midbrain locomotor region pathology. However, gait ignition failure syndrome secondary to lumbosacral spinal stenosis has not heretofore been described.
MethodsCase Study: A 65-year-old right-handed woman underwent a right frontal parasagittal arteriovenous malformation embolization 25 years prior to presentation. After a fall resulting in a T12 and L1 compression fracture, two kyphoplasties were performed. After the second kyphoplasty, one year prior to presentation, she developed new onset of gait ignition failure, left anterior thigh pain, lower back pain at L5 with radiation to both hips, and bilateral lower extremity weakness. The gait difficulty duration correlates to the duration she is in a seated position. Upon standing, she is unable to move her legs and exhibits basophobia, feeling she may fall due to weakness and she is unable to lift up her left foot to initiate gait, as if it is glued to the floor. She is able to initiate gait after one minute, but has an unsteady scissors-gait for the first few steps. Afterwards, her gaitreturns to baseline. Anteroflexion was noted to eliminate her back and leg pain.
ResultsGait examination shows inability to initiate gait after standing, feeling as if frozen. However, she demonstrated scissors-gait after 30 seconds for 3-5 steps, which gradually improved to baseline. Her quadriceps femoris reflex was absent on the right, 3+ on the left. Her Achilles reflex was absent on left. MRI indicated spinal stenosis with broad based osteophytes at T9-T12 and bilateral neural foraminal stenosis at L1-S1. Exercise therapy designed for spinal stenosis was initiated, and resulted in elimination of gaitignition failure.
ConclusionGait ignition failure syndrome may not be necessarily due to frontal or midbrain dysfunction, but can be secondary to lumbosacral impairment. In this patient, dysfunctional arachnoid villi in the lumbosacral nerve roots may have led to transient increases in pressure throughout the neural axis, including the brain, and associated NPH-like symptoms, such as magnetic gait. Seeing that posture affects epidural pressure in lumbar spinal stenosis, with a decrease pressure in response to anteroflexion and reduced pain [Takahashi 1995], one can postulate that this may be a mechanism affecting the patient. Furthermore, since her symptoms are episodic and directly associated with the duration of time she is seated, one may deduce gait ignition failure to be a manifestation of cerebrospinal fluid or intracranial pressure changes influenced by posture. In addition, symptom resolution via exercise therapy strongly suggests that gait apraxia can also be a manifestation of lumbosacral dysfunction. Therefore, those with gait ignitionfailure syndrome warrant evaluation for lumbosacral pathology.
Funding AcknowledgementsSmell and Taste Treatment and Research Foundation.
136 CerefolinNAC Therapy-Induced Dizziness
- Jasir T. Nayati, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 23 / Issue 1 / February 2018
- Published online by Cambridge University Press:
- 15 June 2018, pp. 85-86
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Study Objective
CerefolinNAC (CFLN-NAC) contains L-methylfolate (6 mg), methylcobalamin (2 mg), and N-acetylcysteine [NAC] (600 mg) [Pamlab 2017]. Dizziness and lightheadedness have not heretofore been described with use of CFLN-NAC.
MethodsCase Study: A 64 year old right-handed female was started on CFLN-NAC for smell and taste issues. Over a three day period, she experienced a gradual increase in dizziness. This was a non-vertiginous lightheadedness, so severe that she was unable to walk, and would lie down the entire day to alleviate the dizziness. It was associated with nausea, but without any vomiting or falls. The dizziness would come and go, last for several hours, and was 9/10 in severity.
She admits to a past history of epochs of vertigo. The vertigo occurred three times with nausea and vomiting 13 years, 11 years, and 4 years prior to presentation. She also developed a constant, bilateral, high-pitched tinnitus 14 years prior to presentation, which obstructs her hearing. It is level 3/10 in intensity during the night and in the quiet. There were no alleviating or aggravating factors. Acupuncture was without effect, and she denies any ear pain. After ceasing CFLN-NAC for three days, a gradual reduction of dizziness to baseline ensued.
ResultsAbnormalities in Physical Examination: General: Decreased blink frequency and hypokinesia. Cranial Nerve III, IV, VI: Saccadization of horizontal eye movements. Motor Examination: Tone: 1+ cogwheel rigidity in both upper extremities, left more than right. Drift Test: Bilateral Abductor Digiti Minimi sign with cerebellar spooning. Reflexes: Absent quadriceps femoris and Achilles bilaterally. Positive Hoffman reflex bilaterally. Neuropsychiatric Testing: Go-No-Go Test: 6/6 (normal). Animal Fluency Test: 19 (normal). Reliable Digit Span: 10 (normal). Clock Drawing Test: 4 (normal). Center for Neurologic Study Lability Scale: 10 (normal). Other: Audiometry and Fiberoptic Endoscopy: normal. MRI of the brain with and without contrast was normal.
ConclusionNone of the individual components in CFLN-NAC have been reported to precipitate dizziness [Pamlab 2017]. The non-vertiginous nature of the dizziness makes it unlikely to be due to vestibular involvement, raising the spectre of this drug having an impact on the autonomic nervous system. While a nocebo effect could be in action, this is unlikely since dizziness was not presented as a potential side effect on initiation of the medication. In addition, methylcobalamin can cause hyperviscosity syndrome, but due to an absence of visual disturbances and altered mental status, it is also improbable. The relatively rapid onset with initiation and resolution upon discontinuation of this medication strongly suggests that it is not a coincidence, rather an origin for the dizziness. Those who are treated with CFLN-NAC should be queried as to new onset dizziness. For those already dizzy, one should consider other treatment options.
Funding AcknowledgementsSmell and Taste Treatment and Research Foundation
124 Epochs of Anosmia and Ageusia in Multiple Sclerosis: Chemosensory Uhthoff’s Phenomenon
- Davinder Dhillon, Jasir T Nayati, Priya Batta, Alan R. Hirsch
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- CNS Spectrums / Volume 23 / Issue 1 / February 2018
- Published online by Cambridge University Press:
- 15 June 2018, pp. 78-79
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Study Objective
To reveal that while long duration of anosmia and ageusia has been seen with Multiple Sclerosis (MS) [Doty 1997], repetitive shorter epochs ofanosmia and ageusia has not heretofore been presented.
MethodsCase Study: A 39 year old right-handed male, with a history of MS, presents with six years MS concurrent with epochs of anosmia and ageusia. The anosmia andageusia present concurrently, preventing him from smelling and tasting his meal. At baseline, he is able to smell and taste coffee, peppermint, gum, sweet and salty foods, rating his smell and taste at 70% normal. However, during the epochal events, he reports the inability to smell and taste white rice, shrimp, meat, butter, carrots, onions, spinach, and sour foods. He states that these episodes occur approximately ten times a week, last for two hours, and rates his smell and taste from 0-10% during these events.
ResultsAbnormalities Neurological Examination: Cranial Nerve (CN) Examination: CN II: bilateral pale discs. CN III, IV, VI: bilateral ptosis. CN IX, X: decreased gag reflex bilaterally. Motor Examination: Drift Test: positive left pronator drift, with right adductor digiti minimi sign and right cerebellar spooning. Sensory Examination: Ipswich Touch Test: decreased in left lower extremity. Temperature: decreased in left lower extremity. Rydel-Seiffer Vibratory Test: bilateral upper extremities 5 and bilateral lower extremities 3. Tandem Gait: unstable. Cerebellar Examination: Holmes Rebound Phenomena: positive with left greater than right. Reflexes: 1+ bilateral upper extremities, absent bilateral lower extremities. Neuropsychiatric Examination: Animal Fluency Test: 15 (abnormal). Clock Drawing Test: 3 (abnormal). Center for Neurologic Study Lability Scale: 16 (pseudobulbar affect).
ConclusionPrimary olfactory dysfunction with secondary inhibition of retronasal smell and perceived taste [Gruss 2015] can be an etiology. Such an olfactory dysfunction may reflect variation in nasal mucosal engorgement due to normal variability of the olfactory cycle [Eccles 1978]. This phenomenon is an unlikely due to the short duration ofepochs.
The cause of anosmia and ageusia in this patient suggests a central lesion involved in the processing of both smell and taste. Transient rapid symptoms associated with temperature change, as in Uhthoff’s phenomenon seen in MS, can manifest with deficiency in special senses including visual field loss [Davis 2010]. Such also may be the origin for the chemosensory loss seen here. While this phenomenon may be induced by hot baths, more subtle temperature changes may also induce such symptoms [Romani 2000]. Given that olfactory threshold changes have been demonstrated in acute inflammatory changes in MS, such a temperature related etiology is more likely to manifest [Lutterotti 2011]. MS patients should be screened for chemosensory dysfunction, and those with chemosensory dysfunction should be assessed for demyelinating disease.
Funding AcknowledgementsSmell and Taste Treatment and Research Foundation