44 results
The Bitter Touch: Acquired Tactile-Gustatory Synesthesia
- Sabina Sadana, Raunaq Singh Ratra, Harman Kainth, Pukhraj Singh Nijhar, Manmeet Singh Sahni, Alan Hirsch
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- Journal:
- CNS Spectrums / Volume 28 / Issue 2 / April 2023
- Published online by Cambridge University Press:
- 14 April 2023, p. 258
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Introduction
Gustatory sensation in response to tactile stimulation has been reported to occur in only 0.6% of synesthetes and has rarely been formally described.
MethodsCase Study: A 29-year-old female with schizoaffective disorder – depressed subtype, two months prior to presentation, began noticing that when she touched objects, she would experience an abnormal taste in her mouth. When she would touch specific items with her fingertips, for instance wood, bedsheets, tables, cups, plates, silverware, metal, trash cans, and toothpaste would induce a bitter taste. Touching wood caused the most intense bitter taste. Touching glass did not precipitate a taste.
ResultsMental Status Examination: Disheveled and guarded with minimal eye contact. Anxious and agitated. She believes people are stalking her and that cell phones, radios, and computers emit radiation which makes her head burn as if it is on fire. She perceived that inanimate objects, such as furniture, were staring at her. Other: CT scan of brain with and without contrast: normal.
DiscussionThis could be due to neural overactivation between brain regions due to a neighborhood effect, with cross-firing of connecting fibers. The cortical taste area of the brain lies within the Brodmann area 43 of the parietal lobe which includes the pre- as well as post-central gyri extending into the parietal operculum. Brodmann areas 3, 1, and 2 in the postcentral gyrus is where the primary sensation for touch is mediated. The stimulation in adjacent and overlapping anatomical structures may be explained by ephaptic transmission with firing of one causing discharge of the second, yclept the adjacency principle.This co-localization hypothesis is further supported by the occurrence of pathological state of seizures which manifest both tactile and gustatory sensation. Such a hypothesis would be supported by Anderson’s 1886 observation discussing a peculiar sensation in the right arm and hand elicited concurrently with a bitter sensation in the mouth. Through an overflow phenomenon, touch may induce a diffuse serotonergic discharge to more remote regions of the brain that may mediate their functions through serotonin, such as taste. Possibly, other pathology may be invoked to explain this synesthesia. A deprived sensory system may be hyper-receptive to stray or overflow of sensations which are then interpreted within the sensorily deprived sensory system, as in Charles Bonnet syndrome. In the chemosensory sphere, sensory deprivation is associated with chemosensory hallucinations. If the patient manifests gustatory deficit, it may have predisposed her to sensitivity to such stray or overflowing sensory stimulus from touch manifesting as gustation. In those who present with synesthesia, investigation of pathology in the sensory system of the receiving concurrent sensation is warranted.
FundingNo Funding
Vilazodone-Induced Glycolimia
- Maria de Guadalupe Jimenez Ayasta, Alan Richard Hirsch
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- CNS Spectrums / Volume 28 / Issue 2 / April 2023
- Published online by Cambridge University Press:
- 14 April 2023, pp. 245-246
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Introduction
Glycolimia is observed in a plethora of medical conditions including burning mouth syndrome, opioid withdrawal, as well as from a variety of medications including vortioxetine, l-methylfolate, lisdexamfetamine, and gabapentin. While vilazodone, an antidepressant with agonist like effects on 5-HT1A receptors, has been found to induce hyperglycemia, it has not heretofore been reported to induce glycolimia. Such a case is described.
MethodCase study: A 60-year-old, left-handed (pathological) male presented with a past history of depression, minimally responsive to a variety of antidepressant medications, was begun on vilazodone, initially 20 mg and gradually increased to 60 mg a day. On 60 mg a day he noticed severe cravings for sweets, which he had never experienced prior to starting vilazodone. He found he had increased consumption, craving sweet foods including cookies and candy. For instance, in a typical day, he would eat eight Oreos, chocolate-covered graham crackers, one pint of ice cream a day, and he would crave sweets even after feeling satiated after consuming a meal. Along with this increased eating, he gained 20 pounds over the 3 months while on the vilazodone. Upon discontinuing the vilazodone, although the weight didn’t change, the sweet cravings resolved.
ResultsAbnormalities on: Neurological examination: Mental status examination: Immediate recall: able to remember 6 digits forwards and 3 digits backwards. Motor examination: Drift testing: right inward drift. Gait examination: unstable tandem gait. Neuropsychiatric examination: Go-No-Go test: 6/6 (normal). Animal Fluency Test: 22 (normal).
DiscussionThere are myriad mechanisms whereby vilazodone may have induced glycolimia. Possibly due to its antidepressant effects, it increased hedonics, generating appetitive behaviors, including enhanced socialization, sexual, and other consumptive behaviors, including eating. Peradventure it may have enhanced motivation and socialization. Along with socialization, there is escalation in social intercourse, with accompanying commensalism. Along with such consumptive behaviors, we could anticipate glycolimia. As a 5-HT1A receptor agonist, possibly vilazodone may have acted on the arcuate pro-opiomelanocortin neurons associated with hyperphagia, with modulation of energy homeostasis in the serotonin pathway. Alternatively, vilazodone may have triggered an enhanced insulin response with secondary reduction in blood sugar, leading to a homeostatic behavioral response of increased glucose intake. In those who are treated with vilazodone, query as to glycolimia is warranted and warning as to potential manifestations of hyperglycemia should be entertained.
FundingNo Funding
Pure Verbal Autopalinacousis
- Alisa Trinh, Alan Hirsch
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- CNS Spectrums / Volume 28 / Issue 2 / April 2023
- Published online by Cambridge University Press:
- 14 April 2023, p. 215
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Introduction
Palinacousis, the phenomenon in which sounds are internally perseverated or repeated has not heretofore been reported occurring exclusively to an individual’s own voice.
MethodsA 52-year-old woman started to experience auditory hallucinations of her voice at 3 years old when she began talking out loud. The auditory hallucinations of her own voice, yclept autopalinacousis, consisting of one to three words, were affectively neutral, rarely disruptive, and unchanged by psychiatric medications. During these palinacoustic phenomena, she would hear the last few words she had spoken out loud repeat inside her head in both ears. When the autopalinacousis occurred, the words were repeated just once. Sound quality was an exact replication of how it was originally spoken. She only experienced the palinacousis to her own voice and never to any other sounds. For the palinacousis to occur, she had to verbally state the words loud enough for her to hear. If she spoke out loud but could not hear her own voice, via occlusion of her external auditory canal or presence of loud noise, the internal auditory repetition would not occur. However, after the auditory stimulus was sensed, nothing could reduce the palinacousis. The palinacousis could occur if she read out loud, but not if she read silently. The frequency of the autopalinacousis ranged from a few times a week to several times a day and was associated with reduced sleep, but unaffected by mood, psychiatric medications, or headaches. Five months prior to her psychiatric hospitalization, she began to experience paranoid delusions, decreased sleep, increased activity, rapid speech, and auditory hallucinations of one male and two female voices. In contrast to autopalinacousis, these auditory hallucinations consisted of full phrases or sentences, were affectively charged, intrusive, and diminished by psychiatric medications. No palinacousis occurred with the hallucinated voices.
ResultsAbnormalities: Mental Status Examination: Speech: pressured. Oriented x2. Memory: ability to remember 5 digits forwards and 2 digits backwards. She is not able to spell with word “world.” Calculation ability: poor. MRI of brain with and without contrast: normal.
DiscussionIn cases where patients with psychotic illness experience palinacousis, the palinacousis always appear after the psychotic illness has already manifested, anywhere from less than a year to 15 years later. Our patient’s palinacousis presented almost 5 decades before the onset of her auditory hallucinations and paranoid delusions. Furthermore, her palinacousis only occurred to her own spoken voice and never to any other voices. In those who present with auditory hallucinations, query as to the presence and characteristics of palinacousis is warranted.
FundingNo Funding
These Are Not the Droids You Are Looking For: Mechanical Variant of Cotard’s Syndrome
- Ahmed A. Chaudhry, Syeda A. Shah, Alan R. Hirsch
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- CNS Spectrums / Volume 27 / Issue 2 / April 2022
- Published online by Cambridge University Press:
- 28 April 2022, p. 228
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Introduction
Cotard’s syndrome is a nihilistic delusion where the individual believes they are dead, partly dead, or replaced by an animal. The delusion that their body has been replaced by a purely inanimate azooic (but physical entity), such as a robot or a droid, has not hitherto been described.
MethodsCase study: This 60-year-old, right-handed, female, with a past history of schizophrenia presented with complaints of depression, irritability, and anger. When confronted with commitment papers signed by her father, she denied their truthfulness, insisting that he had been replaced by an imposter. This belief persisted unabated, despite treatment with 20 mg of haloperidol per day. Over time, she expressed the belief that she had been replaced by another person, whom she refused to identify. The following day she refused all food and water proclaiming that she had died and been replaced by a machine revealing, “I am not her. I am a robot.” Soon thereafter she developed tremulousness, stiffness, and rigidity. After haloperidol was decreased and benztropine started, these parkinsonism symptoms subsided, but her delusions persisted.
ResultsAbnormalities in physical examination: General: decreased blink frequency. Neurologic examination: Mental status examination: bradyphrenia, hypoverbal, blunted affect. Oriented ×2. Motor examination: bradykinetic, cogwheel rigidity in both upper extremities. Gait examination: slow shuffling gait, reduced bilateral arm swing. Cerebellar examination: resting tremor in both upper extremities at 3 cycles per second. Other: EEG: focal sharp transients in the left temporal region. MRI with and without contrast: normal. Toxicological, metabolic, endocrine screening: normal.
ConclusionThis illustrated sequential presentations of three delusions of misidentification. Upon presentation, she exhibited Capgras syndrome, the delusional belief that a familiar person has been replaced by a double. The nidus for this may have been the discovery that her father had signed her commitment papers. This was followed by the belief she was a double of herself, which is the syndrome of Reverse Subjective Doubles. Finally, she manifested Cotard’s syndrome in a previously undescribed manner, believing she had died and become a robot. Cotard’s and Capgras syndromes are known to present sequentially rather than concurrently, whereas the patient presented concurrently with all three syndromes. Drug-induced parkinsonism may have made the patient subjectively feel stiff, which she interpreted as being rigid like a robot. She was bradykinetic, did not eat or drink, and had rigidity, suggesting that these were somatic manifestations of her underlying delusion of being a robot or alternatively, may have been the somatic nidus for the delusion. Those who present with Cotard’s syndrome warrant evaluation for underlying medical conditions, serving as a substrate for this delusion.
FundingNo funding
Anosmia as an Enantiopathy for Migraines
- Amrinder Singh, Sidhu Rubani, Estevao Ribeiro, Vikram Preet Kaur, Alan Hirsch
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- CNS Spectrums / Volume 27 / Issue 2 / April 2022
- Published online by Cambridge University Press:
- 28 April 2022, p. 229
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Introduction
Elimination of olfactory sensory perception with a reduction in odor-induced migraine has not heretofore been reported.
MethodsCase study: A 64-year-old right-handed woman presented with a history of common migraines since childhood. The headaches were bilateral, throbbing, pulsatile, and without aura and were associated with lightheadedness, photophobia, sonophobia, nausea, and vomiting. They would be precipitated by ambient aromas, such as perfumes and bath products, and she became agoraphobic, fearful of going out of her domicile and being exposed to odors. She avoided stores, perfume counters, and public places; scared that it would initiate a disabling headache. Twenty-five years prior to presentation, the patient fell on ice, striking her head and causing a transient loss of consciousness and persistent absence of smell and taste. From that point forwards, while she would have an occasional headache independent of an odor, she no longer experienced odor-induced headaches. Her agoraphobia had resolved. Since the head trauma, her smell remained at 10% to 20%. Her taste remained at 30% of normal.
ResultsAbnormalities on neurological examination: Motor examination: Drift testing: Right pronator drift with right abductor digiti minimi sign. Cerebellar examination: Bilateral finger-to-nose dysmetria. Rapid alternating movements: decreased in the left upper extremity. Reflexes: Bilateral upper extremity 3+. Absent bilateral ankle jerks. Bilateral palmomental and Hoffmann reflexes present. Chemosensory testing: Olfaction: Brief Smell Identification Test (B-SIT): 7 (hyposmia), Alcohol Sniff Test: 0 (anosmia). Retronasal Olfaction: Retronasal Smell Index: 4 (hyposmia). Gustation: Propylthiouracil Disc Taste Test: 10 (normogeusia). While performing the B-SIT and sniffing the aroma of rose, the patient noted the sudden onset of a headache, even though she could not detect any odor present.
DiscussionThe temporal relationship between loss of sense of smell and elimination of odor-induced migraines suggests a causal relationship. Conscious recognition of odor may induce a stimulus-response paradigm, whereby migraine occurs. Head trauma-induced anosmia, by elimination of conscious perception of the odor, may thus be the modality whereby her headaches resolved. Alternatively, odors may induce an autonomic response, and conscious recognition of such autonomic response may induce a headache. To tergiversate, that the rose aroma in the B-SIT induced a headache, without any conscious detection of the odor, implies that either unconscious perception is enough to precipitate a headache or that these odors act not as odorants, but rather as an exogenous ambient chemical inducing headaches. Possibly the production of temporary anosmia by use of nose clips may be utilized as a prophylactic device for those with odor-induced migraines. Further investigation into this is warranted.
FundingNo funding
Alliaceous Axilla as a Manifestation of Olfactory Reference Syndrome
- Anton S. Lima, Jenish V. Patel, Tiffany Chang, Alan R. Hirsch
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- CNS Spectrums / Volume 27 / Issue 2 / April 2022
- Published online by Cambridge University Press:
- 28 April 2022, p. 231
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Introduction
Olfactory reference syndrome (ORS) is a delusion in which a person believes that he or she exudes a displeasing body aroma that others perceive negatively. The axilla has been reported as a single primary source in only one patient. Furthermore, ORS is rarely reported to be associated with food odor. In these instances, the food is not edible. Delusions of ORS presenting as alliaceous edible food aromas have not heretofore been described.
Case ReportOne week after undergoing catheter ablation for atrial fibrillation, this 42-year-old right-handed male experienced a sudden onset of loss of smell and taste. This has persisted on presentation and he described a complete lack of smell, only being able to smell different spices and herbs. Over time, his sense of smell selectively improved such that he was able to smell alliaceous substances, including onion and garlic, as well as a few other aromas. At the same time his smell returned, he noted that his own body exuded a smell of garlic. This occurred especially while weightlifting at the gym. He noticed that the shirts he had worn working out, in the axillary regions, were encumbered with a garlic/onion miasma. He was fearful that this mephitic aroma was being secreted through his armpits, and that others would recognize his tragomaschalia. As a result, he restricted his activities. Over a few months, his smell ability gradually worsened back to the condition he was in after the ablation. Coincident with this, his perception that he was exuding an alliaceous aroma resolved.
ResultsMotor examination: Drift testing: mild left pronator drift. Left abductor digiti minimal sign. Olfactory testing prior to the development of ORS: Alcohol Sniff Test (AST): 0 (anosmia). Brief Smell Identification Test (B-SIT): 3 (anosmia). Olfactory testing during ORS: AST: 16 (hyposmia). B-SIT: 9 (hyposmia). Olfactory testing after resolution of ORS: AST: 0 (anosmia).
DiscussionThis could be explained by a physiologic axillary odor or malodor, which he could not detect before or after the ORS. During the ORS, the odor may have been misperceived in a dysosmic manner due to his underlying olfactory deficit. Such dysosmia may have then been interpreted as the aroma of an alliaceous vegetable. The intensity of the aroma may have been greatest at the axillary area if compared to the other sources, but due to his underlying hyposmia, he was able to perceive only the axilla as a sole source of the aroma. Besides, psychodynamic preoccupation with bodily physique may have explained his hypersensitivity to minor flaws and his excessive preoccupation with possible harassment from others. He may have consequently misinterpreted individuals’ benign observations and attitudes to presume the presence of aroma. In individuals with olfactory deficit, this investigation for the presence of ORS with traditionally unpleasant food aromas or the presence of ORS in those with chemosensory dysfunction is warranted.
FundingNo funding
Xylological Variant of Reverse Fregoli Syndrome, Delusions of Being a Tree
- Harsimran Singh Bakhshi, Alan Richard Hirsch
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- Journal:
- CNS Spectrums / Volume 26 / Issue 2 / April 2021
- Published online by Cambridge University Press:
- 10 May 2021, p. 145
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Introduction
The delusion of being a living animate non-animal object has not heretofore been reported.
MethodsA 21-year-old right-handed cisgender female, two months prior to presentation, noted stiffness and difficulty with ambulation. One-month prior to admission, she experienced recurrent depression with myriad vegetative and nonvegetative symptoms of depression. On admission her chief complaint was I am a tree, standing motionless and minimally responding to query. After treatment with quetiapine, mirtazapine and hydroxyzine for a one-week period, her perception of being a tree fully resolved.
ResultsAbnormalities in Mental Status Examination: Anxious mood repeatedly stating, I am a tree. Standing still for long periods of time, refusing blood pressure to be obtained and expressing fear of constricting flow. Neuropsychiatric Testing: Beck Depression Inventory Type II: 33 (severe depression)
DiscussionThe rapid response to risperidone is consistent with Cotard’s syndrome, which has been noted to respond rapidly to neuroleptics (Sharma, 2014). However, in Cotard’s syndrome, replacement by a living non-animal object has not hitherto been reported. Body infestation with animate objects, as in Ekbom syndrome, only includes animals not botanicals (Chaudhary, 2019). This could be viewed as Reverse Inanimate Capgras Syndrome: instead of an imposter replacing a close friend, who then is inserted into the sufferer; a tree has replaced the sufferer. Peradventure, this may fit into the construct of Intermetamorphosis, a misidentification syndrome associated with the belief that individuals have transformed into other persons (Jariwala, 2017). Botanical Intermetamorphosis, the belief by the sufferer that the other individual is transformed from a person into a plant has not been described. Reverse Intermetamorphosis is the projection of an external individual into the person suffering or a syndrome of altered physical and psychological identities of the self (Silva, 1990). However, in this situation, the objects are all human or animate animals not botanicals. In Fregoli syndrome, there is an altered physical identity of others. In Reverse Fregoli syndrome, the sufferer assumes the physical but not the psychological identity of the stranger (Silva, 1990). But in this instance, the stranger is human as opposed to a plant life form. In the current case there is only altered physical identity (into a tree) not psychological identity. The current case may also be interpreted as a Botanical Variant of Interparietal Syndrome. In this condition, parts of the body are perceived to be lifeless, due to lesions of the inferior parietal lobe including supramarginalis gyrus, angular gyrus and the basalis parietalis area (Angyal, 1935). Investigation for those whom have Intermetamorphosis, Fregoli syndrome, Capgras syndrome, Interparietal syndrome, and Cotard’s syndrome for the presence of delusions involving plant life is warranted.
108 Warning: Generic Suboxone Not Equal to Name Brand
- Arvind Datt, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 25 / Issue 2 / April 2020
- Published online by Cambridge University Press:
- 24 April 2020, p. 270
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Introduction:
On June 14, 2018, the FDA approved generic buprenorphine/naloxone, as an alternative to the brand Suboxone (FDA,2018). A patient who developed acute withdrawal symptoms when switched from Suboxone to generic buprenorphine/naloxone at the same dosage, with resolution with replacement with brand name Suboxone, is presented. Induction of withdrawal with generic buprenorphine/naloxone has not heretofore been described.
Methods:Case Study: A 39-year-old right handed single male presented with a past medical history of intravenous heroin dependence. He was relapse free for 5 years and without change on Suboxone film 8mg/2mg twice daily, and was provided with prescriptions for the same, which was substituted to generic brand Dr. Reddy’s Lab SA buprenorphine HCl/naloxone HCl 8mg/2mg film. After two days on this, one hour after taking generic buprenorphine/naloxone film, symptoms of withdrawal began as manifest by hot flashes, diaphoresis, cold chills, leg cramping, and nausea without vomiting. These were the same symptoms he experienced during his past inpatient withdrawal from opioids. These symptoms recurred every day for an entire week until switching back to brand name Suboxone, whereupon his withdrawal symptoms resolved.
Discussion:The mechanism whereby the generic buprenorphine/naloxone combination induced withdrawal symptoms is unclear. It appears that this generic version was either not effectively blocking the mu receptors or the naloxone was inducing a withdrawal state. Possibly the porous nature of the film was such that less of the buprenorphine was absorbed through the mucosa. As a result, less was transferred into the bloodstream, across the blood brain barrier, to the nucleus accumbens, and ultimately on kappa opioid/mu receptor (Centerwatch, 2002). Alternatively, a greater amount of naloxone may have been absorbed transmucosally, thus inducing withdrawal. The absorption may have been normal, but the exact milligram dosage may not be accurate with either too little buprenorphine or too much naloxone. On the other hand, this buprenorphine compound may have been pH sensitive, such that it became inactivated upon exposure to the mildly acidic salivary pH. He could have been malingering this response. Again this is unlikely since he was not given a higher dose of buprenorphine/naloxone, rather the same dose of Suboxone as previously prescribed. It is important that physicians be aware of the possibility for acute withdrawal and increased cravings, which can lead to relapse while using this agent. Further investigation of the efficacy of the generic variant and Suboxone as replacement therapy is warranted.
122 Burning Mouth Syndrome as a Focus of Delusion
- Chevelle Winchester, Alan Hirsch
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- CNS Spectrums / Volume 25 / Issue 2 / April 2020
- Published online by Cambridge University Press:
- 24 April 2020, p. 279
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Parasitosis is a fixed belief of being infested with pathogens against all medical evidence [Freudenmann RW, Lepping P, 2009] Method: Case Report: A 53 year old right handed female presented with progressively severe BMS for 1 years. She noticed that aromas would project from her nose into her mouth and would experience this taste for days. Looking at the source of the odor would precipitate her to sense the smell of the product, immediately followed by the taste and then burning of the tongue, mouth and vagina. Fumes would eminent from her mouth, nose and anus. Five days prior she stopped eating and drinking. She had not brushed her teeth, showered, nor bathed for 3 weeks. Odors smell like ammonia and blood, which upon inhalation, effuse into her mouth which tastes like chemicals. Thereupon, she immediately experiences burning of her tongue and palate.
Results:Abnormalities: Disheveled: Cacosmious. Personal hygiene poor. Facial expression odd and inappropriate. Loud but low quantity of speech. Unable to interpret similarities or proverbs. Calculation: poor.
Conclusion:In those who present with BMS, query as to the delusional nature of their symptoms is warranted and may suggest a treatment strategy.
121 Oviposit Dysgeusia; Head Trauma Induced Chemosensory Noisome Egg Dysgeusia: The Miasma of Dante’s Inferno-When Eggs Become Rotten
- Chevelle Winchester, Alan Hirsch
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- Journal:
- CNS Spectrums / Volume 25 / Issue 2 / April 2020
- Published online by Cambridge University Press:
- 24 April 2020, pp. 278-279
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Introduction:
Post-traumatic dysgeusia with conversion of the taste of eggs rotten eggs has not heretofore been described.
Method:Case Report: A 60 year old right handed female 6 months prior to presentation sustained head trauma. Three days later she noted reduced taste and smell dysgeusia to eggs. Eggs tasted distorted, like rotten eggs. Raw egg whites had no smell or taste. Cooked egg whites had faint sulfur smell for 2-3 seconds and the taste of sulfur. Yolk of soft-boiled eggs, had no smell or taste. The white had no smell but an unbearable sulfur taste. Raw eggs had no smell. The yolk of hardboiled eggs had no smell and taste, the whites smelled and tasted like sulfur. Sunny side up eggs with yolk and white segregated had no smell but tasted, as they should. Sunny side up eggs with yolk and white mixed together has no smell but strong sulfur taste. Scrambled eggs had no smell but mild sulfur taste, which changed over time to a rotten egg smell and taste. With nose clips, scrambled eggs had 0/10 taste, without the nose clips the smell of sulfur was 3/10.
Results:Olfaction: Normosmia to threshold and Retronasal Smell Index: 2 (abnormal): Gustatation : Normogeusia to all. Mild hypogeusia to sodium chloride. MRI: Multiple foci of periventricular and deep white matter demyelization.
Discussion:Rotten egg smell maybe mediated through retro-nasal pathways, since nasal obstruction eliminated the rotten egg taste. Eggs can possibly be developed as a home device to assess chemosensory function.
101 Amyotrophic Lateral Sclerosis (ALS) - Not Just a Motor Disease? Isolated Bitter and Sweet Taste Loss in ALS
- Ahmed A Ashary, Dev N Patel, Alan R Hirsch
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- CNS Spectrums / Volume 25 / Issue 2 / April 2020
- Published online by Cambridge University Press:
- 24 April 2020, p. 266
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Study Objective:
Specific taste quality deficits in ALS has not heretofore been described.
METHOD:Case Study: A 71 year old right handed female presented with a two year course of progressive reduction in strength in her hands, arms and legs with difficulty tying shoe laces, opening jars, writing and walking. She described nocturnal muscle spasms involving all extremities. Gradually, over eight months prior to presentation, all food began to taste bad and horribly bitter. Associated with no appetite and a seven pounds weight loss.
RESULTS:Abnormalities in Neurological examination: Cranial Nerve (CN) examination: CN IX and X: Gag absent bilaterally. Motor examination: Bulk: atrophy in thenar and hypothenar eminences and intrinsics in both upper extremities. Percussion induced fasciculation and myotonia in both shoulders and arms. Fasciculation of tongue with percussion myotonia of tongue. Strength: Intrinsic 4/5 in both upper extremities, 3/5 in abductor policis brevis bilaterally, 3/5 right gastrocnemius soleus, 4/5 bilateral anterior tibialis. Drift testing: left abductor digiti minimi sign. Gait: Heel and toe walking unstable with circumduction of left leg. Tandem gait unstable. Cerebellar: Holmes rebound phenomena positive in the left upper extremity. Deep tendon reflexes: 1+ left brachioradialis. 1+ left triceps. 3+ right ankle jerks. 0 left ankle jerk. Positive jaw jerk. Chemosensory Testing: Normosmia to: Alcohol Sniff Test (46), Pocket Smell Test (3/3) and Retronasal Smell Index (9). Taste Quadrant Testing: ageusia in the palate to sodium chloride and citric acid. Ageusia throughout the palate, tongue and whole mouth to sucrose and quinine hydrochloride. Fungiform papillae count: left 18, right 20 (normal). Lip biopsy (normal). MRI: T2 flair in bilateral corticospinal tracts, left greater than right in the spinal cord and the brain. EMG: fibrillation, positive waves with fasciculation in all four extremities. Voluntary contraction with polyphasic unstable motor unit action potentials.
CONCLUSION:While Lang found no taste loss in ALS (Lang, 2011), Pelletier found reduction in intensity of taste to all modalities in different sectors of the tongue, but paradoxically demonstrated normogeusia in whole mouth taste perception (Pelletier, 2013). Pathological specimens of those with ALS revealed degeneration in the nucleus parabrachialis medialis and tractus trigeminothalamicus dorsalis (Oyanagi, 2015), suggesting that taste deficit may be due to central white matter abnormalities. Sweet taste is localized in the most posterior and rostral aspect of the right insular cortex, immediately adjacent to bitter (Prinster, 2017), suggesting a neighborhood effect phenomena. Weight loss in ALS may be due to sensory distortion and secondary impairment of appetite. It would be worthwhile to investigate those with ALS for evidence of otherwise overlooked gustatory deficits, correction of which may improve appetite and nutritional state.
131 A Marionettist Pulling My Strings: A Case of Buprenorphine-induced Chorea
- Dev Patel, Ishandeep Gandhi, Faisal Malek, Camille Olechowski, Alan R. Hirsch
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- Journal:
- CNS Spectrums / Volume 25 / Issue 2 / April 2020
- Published online by Cambridge University Press:
- 24 April 2020, pp. 282-283
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Introduction:
Choreaform movements provoked by opiates is an infrequent adverse event. Buprenorphine induction of chorea has not heretofore been described. Such a case is presented.
METHOD:Case Study: A 38-year-old female presented with a decade long history of alcohol, cocaine, benzodiazepine, and heroin abuse. The patient was insufflating 1.5 grams of heroin daily. On presentation, she was actively withdrawing, scoring 17 on the Clinical Opioid Withdrawal Scale. Urine toxicology screening was positive for opiates, cocaine, and cannabinoids. Buprenorphine 4 mg sublingual was initiated. Within one hour, she observed, “My legs were moving uncontrollably as if I was a marionette.” These dance-like movements were isolated to both legs and gradually resolved after discontinuation of buprenorphine: most of the movements manifested in the first 8 hours, and dissipated over the next 2 days. She did have similar movements after treatment with quetiapine during a previous hospitalization, years earlier.
RESULTS:Abnormalities in physical examination: General: goiter, bilateral palmar erythema. Neurological examination: Cranial Nerve (CN) Examination: CN I: Alcohol Sniff Test: 2 (anosmia). Motor Examination: Drift testing: mild right pronator drift. Reflexes: 3+ bilateral lower extremities. Neuropsychiatric Examination: Clock Drawing Test: 3 (abnormal). Animal Fluency Test: 18 (normal). Go-No-Go Test 6/6 (normal).
DISCUSSION:Buprenorphine induced chorea could be a result of partial mu-opioid agonism, or kappa and delta receptor antagonism (Burke, 2018; Cowan, 1977). Mu-opioid receptor activation causes increased dopamine turnover in the nigrostriatum, which is responsible for locomotor sensitization (Campos-Jurado, 2017). With the addition of mu-opioid receptor modulation of dopamine release, kappa-opioid receptor alters various neurotransmitters in the basal ganglia, potentiating hyperkinetic movements. Buprenorphine’s choreiformogenic action may be due to kappa-opioid receptors ability to augment neurotransmission in the striatum (Escobar, 2017; Bonnet, 1998). The combination of simultaneous activity of these three opioid receptors may cause chorea, since they act to modulate dopamine, glutamate, and GABA in the direct and indirect pathways within the basal ganglia (Abin, 1989; Cui, 2013; Allouche, 2014; Trifilieff, 2013). This patient’s history of heroin and cocaine use may have caused supersensitization of dopamine receptors (Memo, 1981), provoking hyperkinesia. Involvement of substance-induced sensitization with concurrent kappa-opioid receptor neurotransmitter augmentation in direct and indirect pathways in the basal ganglia may have primed our patient to the development of chorea after buprenorphine administration. Further investigation for the presence of extrapyramidal movements in those undergoing buprenorphine treatment is warranted.
Standards of Practice in Acute Ischemic Stroke Intervention International Recommendations
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- Laurent Pierot, Mahesh Jarayaman, Istvan Szikora, Joshua Hirsch, Blaise Baxter, Shigeru Miyachi, Jeyaledchumy Mahadevan, Winston Chong, Peter J. Mitchell, Alan Coulthard, Howard A. Rowley, Pina C. Sanelli, Donatella Tampieri, Patrick Brouwer, Jens Fiehler, Naci Kocer, Pedro Vilela, Alex Rovira, Urs Fischer, Valeria Caso, Bart van der Wort, Nobuyuki Sakai, Yuji Matsumaru, Shin-ichi Yoshimura, Luisa Biscoito, Manuel Pumar, Orlando Diaz, Justin Fraser, Italo Lifante, David S. Liebeskind, Raul G. Nogueira, Werner Hacke, Michael Brainin, Bernard Yan, Michael Soderman, Allan Taylor, Sirintara Pongpech, Karel Terbrugge
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- Journal:
- Canadian Journal of Neurological Sciences / Volume 46 / Issue 3 / May 2019
- Published online by Cambridge University Press:
- 20 March 2019, pp. 269-274
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After five positive randomized controlled trials showed benefit of mechanical thrombectomy in the management of acute ischemic stroke with emergent large-vessel occlusion, a multi-society meeting was organized during the 17th Congress of the World Federation of Interventional and Therapeutic Neuroradiology in October 2017 in Budapest, Hungary. This multi-society meeting was dedicated to establish standards of practice in acute ischemic stroke intervention aiming for a consensus on the minimum requirements for centers providing such treatment. In an ideal situation, all patients would be treated at a center offering a full spectrum of neuroendovascular care (a level 1 center). However, for geographical reasons, some patients are unable to reach such a center in a reasonable period of time. With this in mind, the group paid special attention to define recommendations on the prerequisites of organizing stroke centers providing medical thrombectomy for acute ischemic stroke, but not for other neurovascular diseases (level 2 centers). Finally, some centers will have a stroke unit and offer intravenous thrombolysis, but not any endovascular stroke therapy (level 3 centers). Together, these level 1, 2, and 3 centers form a complete stroke system of care. The multi-society group provides recommendations and a framework for the development of medical thrombectomy services worldwide.
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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- 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
61 Heroin Dependence as an Enantiopathy to Quetiapine-Induced Restless Leg Syndrome
- Emma Moghaddam, Edward Lichtenshtein, Sima Patel, Nikhil Rana, Rohan Rana, Alan R. Hirsch
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- CNS Spectrums / Volume 24 / Issue 1 / February 2019
- Published online by Cambridge University Press:
- 12 March 2019, p. 207
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Introduction
Use of heroin in self-management of Restless Leg Syndrome (RLS) has not heretofore been described. Such a case is presented.
MethodsCase study: This 29 years old right handed male presented with a long history of major depressive disorder, generalized anxiety disorder and opioid dependence. The Patient felt compelled to take quetiapine since was the only drug found to be effective in controlling racing thoughts, Major Depressive Disorder with psychotic features. Prior to use of quetiapine the patient never experienced RLS. Quetiapine in doses ranging from 25mg to 300mg a day precipitated severe RLS whereby he was forced to move his leg all night long leading to poor sleep quality. The RLS was unresponsive to Gabapentin and Benztropine, however it was eliminated with a variety of opioids including hydrocodone, buprenorphine, buprenorphine/naloxone. Particularly sensitive to heroin, 1/2 twenty dollar bag, self-administered IV prior to sleep eliminated the RLS immediately, but when injected more than four hours before sleep it had no effect. RLS acted only when induced with quetiapine, since he wished to continue quetiapine to control his mood, he felt compelled to self-medicate with heroin to stop RLS side effects. He showed no other signs of extrapyramidal symptomatology or evidence of any other movement disorder.
ResultsAbnormalities in physical examination: General: Abundance of tattoos on body and face. Cranial Nerve (CN): CN I: Alcohol Sniff Test: 7cm (anosmia). CN II: Anisocoria OD 5mm OS 2mm. Motor Examination: drift testing: right pronator drift. Cerebellar: Finger to Nose: end point dysmetria bilaterally. Low amplitude high frequency tremor in both upper extremities on extension. Sensory Examination: decreased graphesthesia in both upper extremities. Reflexes: 3+ knee jerks, absent ankle jerks, positive jaw jerk, bilateral palmomental reflex is present.
DiscussionThis patient has a long history of quetiapine use due to his major depressive disorder with psychotic features and subsequent self-administration of IV heroin reportedly to reduce the symptoms of quetiapine-induced RLS. Heroin elevates dopamine levels in forebrain by blocking inhibitory GABA interneurons near the ventral tegmental area, leading to activation of mesocorticolimbic dopaminergic neurons (Nakagawa 2008, Steidl 2011). The time frame of opioid administration has a critical impact on its efficacy in improving RLS symptoms. However, the drug’s effects only up to 3 to 6hours (Buchfuhrer 2012). In this case administration of heroin more than 4hours before sleep would not alleviate the RLS symptoms. Patient chose the time of injection, not for hedonic pleasure of heroin, but rather to prevent RLS symptoms. In those with heroin dependence, the possibility that is a result of self-medication of underlying movement disorder warrants additional investigation. In those with RLS who are unresponsive to other treatment modalities, a trial of opioids maybe worthwhile.
24 CerefolinNAC Therapy-Induced Dysgeusia
- Jasir T. Nayati, Fizah S. Chaudhry, Tajinder Parhar, Ather M. Ali, Alan R. Hirsch
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- 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
36 Too Scared to Blink: Pseudoparkinsonism due to Nyctophobia
- Khurram Janjua, 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. 194-195
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Introduction
A hallmark of Parkinson’s disease is facial akinesia with decrease in blink frequency (Karson, 1984). A markedly decreased blink frequency from nyctophobia, a fear of the dark, has not heretofore been reported.
MethodCase Study: A 26-year-old right handed male presented with a 20-year history of phantasmagoria. Visual hallucinations of strangers appeared several to a hundred times a day, seconds to minutes in duration. These morbid images were horrific, of dead people or ghosts, suddenly appearing in his visual space, actively attacking real people. Examples included a little girl, decapitated, cradling her head in her arm or Freddy Krueger like apparitions, shooting, stabbing, strangling or maiming actual people who were within the patient’s visual field. He was able to differentiate between the hallucinations and real people, either from the context (a non hallucination would not be murdering someone else), or he would wait for the hallucinations to vanish, allowing him to then interact with the person who is actually there. The images were so disturbing to him that he fled his home state to run away from the hallucinations, but to his chagrin, they persisted. There were diurnal variations to his hallucinations, which were more frequent at night, or when he closed his eyes, and the fear of these has induced nyctophobia. In order to avoid these, he attempted to curtail closing his eyes or blinking. He had been treated with 9 different psychotropic medications, which had no effect on his hallucinations. Phenytoin was begun, and once therapeutic levels were achieved, all of his hallucinations resolved, as did his nyctophobia, with return to normal blink frequency.
ResultsPhysical examination: Bilateral palmar erythema. Facial expression with decreased blink frequency, approximately 1/per minute, but not otherwise hypomimetic. Neurological examination: Cranial Nerve (CN) Examination: CN III, IV and VI: bilateral ptosis. Motor Examination: Normal tone without cogwheel rigidity. No bradykinesia. Drift Testing: Right upward-outward drift, right cerebellar spooning, and Abductor Digiti Minimi sign. Gait: Normal without instability or retropulsion. Reflexes: 1+ throughout. Hoffman Reflex: positive bilaterally. Other: Magnetic Resonance Imaging of brain with/without infusion: Normal. Five-day Electroencephalogram: Temporal Lobe Status Epilepticus with bilateral foci.
DiscussionIn this individual, the sheer terror of phantasmagoria with his eyes closed, forced him to maintain them in the open position as long as possible, reducing his blink frequency to once a minute or less. The return to a normal rate of blink frequency with treatment using phenytoin, with resolution of his horrific hallucinations, further validates this as the origin for his infrequent blinking. In those with low nictation, without other manifestations of Parkinson’s disease, query as to volitional inhibition of blink frequency and nyctophobia is warranted.
96 The Cat’s Meow? Feline Warning of Imminent Seizures
- Chevelle R. Winchester, Emeto B. Chioma, 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. 222-223
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Study Objective
Cats may respond to seizures with a threat response (Strong, 1999). Detailed description of this for seizures or pseudoseizures has not heretofore been described.
MethodCase study: A 29-year-old right handed female, two years prior to presentation, developed onset of seizures which last approximately one minute, almost on a daily basis. These are associated with shortness of breath and postictal blurred vision. During these epoch, she would experience temporary amnesia; a feeling as if she had lost a couple years of memory which gradually returned within an hour. Pain and stress would precipitate a seizure. There were two different types of seizures. The first type was with an aura of white visual entopias in the center of her visual field without postictal amnesia. The second type is without aura, but there is amnesia for the event. In neither type would she bite her tongue nor manifest urinary or fecal incontinence. Just preceding either type of seizures, her cat, would uncharacteristically meow, saunter over to her, and nudge her head against her legs or scratch her with her front paws. In response to this, the patient would move as fast as she could to a safe place where she would be cushioned if she were to fall. Less than a minute after the cat would warn her, a seizure would manifest. During this event the cat would meow and lay beside her “as if guarding me” until the seizure would resolve. The cat has never displayed these behaviors unless a seizure was eminent. She admitted to daily panic attacks which the cat appeared to ignore.
ResultsAbnormalities in physical examinations: General: 1+ bilateral pedal edema. Neurological examination: Mental status examination: Digit span: 7 forward and 2 backwards. Able to spell the word “world” forwards but not backwards. (CN) examination: CN III, VI and IV: Right lateral rectus weakness. Reflexes: bilateral 3+ brachioradialis and quadriceps femoris. Absent ankle jerk. Positive jaw jerk with clonus. Bilateral positive Hoffman’s reflexes. Neuropsychiatric testing: Clock drawing test: 3 (abnormal). Go-No-Go Test: 6/6 (normal). 72-hour EEG normal.
ConclusionOlfactory emanations occur (Brown, 2011) several hours prior to seizures (Litt, 2009; Rajna, 1997) which the feline may be sensitive due to its superior olfactory ability. The cat’s comportment may have induced anxiety in the patient, which then may have precipitated the seizure. The animal thus may be an epileptogenic animal rather than a warning animal. The cat may detect changes in emotion, which predicts the pseudoseizures. On the other hand, the cat may have been acting as an anxiogenic agent, precipitating a pseudoseizure. There may have been a misattribution error, such that she recalled the cat in a position of warning seizures but did not recall when the cat did not warn the seizures. Further investigation in the use of alarm cats as warning for imminent seizures is warranted.
97 My Inner Blizzard: Effect of Weather on Multiple Sclerosis Exacerbation
- Chevelle R. Winchester, Priya Batta, Dhillon Davinder, 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. 223
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Study Objective
Exacerbation of Multiple Sclerosis (MS) symptoms prior to weather change has not heretofore been described.
MethodsCase Study: A 60 year old right handed female with lifelong anxiety and four years of depression presented with a 20 year history of MS manifested by bilateral lower extremity pain and weakness and urinary incontinence. Since the onset, she observed that approaching storms or weather changes cause her symptoms to worsen. This manifests one day prior to the meteorological shifts of rain or snow. This occurs whether she is at home or on vacation and unlike the weatherman, “she is never wrong.” The aggravation of symptomatology would consist of worsening leg pain and weakness of both lower extremities so that her functional status changes from using a cane to a wheelchair. These symptoms begin one day prior to the storm and gradually worsen to the point of maximum intensity as the storm arrives. The baseline pain is usually 5/10 in severity but with the storm it increases to 8/10. The pain, which progressively worsens as the storm advances, is a vice-like numbness in her shins and spasm in her legs. The pain and weakness will persist for as long as the storm lasts. The pain diminishes and the motor symptoms improve six hours after the storm is over. She can differentiate approaching snow or rain such that snow causes more intense symptoms. She denies change in symptomatology on airplanes or when she is present at high altitude such as Las Vegas or Colorado. She also affirms that her symptoms are worse when she is in a hot tub and better in a cold-water bath. She reports that there is a family history of similar ability to predict the weather in a cousin and nephew, both who also suffer from MS.
ResultsAbnormalities in Neurological Examination: BP 159/115. Pulse 100. Mental Status Examination: disheveled. Depressed mood with congruent affect. Short-term memory: 5 digits forwards, 2 digits backwards. Recent memory: able to recall none of 4 objects in 3minutes without improvement with reinforcement. Unable to interpret similarities or proverbs. Poor ability to calculate. Reflexes: 3+ bilateral lower extremities. Clock Drawing Test: 1 (abnormal).
ConclusionsUhthoff’s phenomena (hot bath test) is well described in MS (Humm, 2004), however the worsening of symptoms prior to weather change has not been reported. Possible mechanisms include meteorological induced anxiety and depression with associated exacerbation (Ackerman, 1998). Other possible mechanisms include misattribution, selective recall, or a misreporting due to psychological needs for acceptance by examiner, similar to the Hawthorne effect (observer effect) (Adair, 1984). With the approaching storms there could be a change in internal temperature, which then preferentially affects areas of demyelination (Kudo, 2014). It is worth querying those with epoch associated neurological disorders as to linkage with meteorological events.
82 Ice Melts Phantogeusia: Cold Inhibition of Gustatory Hallucinations
- Suhanna Mutti, Alan R. Hirsch
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- CNS Spectrums / Volume 24 / Issue 1 / February 2019
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- 12 March 2019, pp. 216-217
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Introduction
Relief of phantogeusia through ice cube stimulation has not heretofore been noted.
MethodsThis 70-year-old left handed (familial) female noted the onset, three and a half years ago, of reduced taste 80 percent of normal, distorted taste, hallucinated metallic taste, and BMS. Upon application of an ice cube to the tongue, both the metallic taste and the BMS resolved for a few seconds, without impairing her true taste ability. With repeat application, the alleviation effect persists.
ResultsAbnormalities in Neurologic Examination: Sensory Examination: Decreased pinprick and temperature bilateral lower extremities. Reflexes: 3+ throughout. Bilateral positive Hoffman’s reflexes. Chemosensory testing: Olfaction: Brief Smell Identification Test: 9 (normosmia). Retronasal Smell Index: 10 (normosmia). Gustation: Propylthiouracil Disc Taste Test: 5 (normogeusia).
DiscussionTransient Receptor Potential 5, is expressed in tongue taste buds, facilitating sweet perception, and is temperature dependent (Fujiyama, 2010). Ice may act to reduce such sweet taste receptor discharge, causing an imbalance in taste fiber discharge thus inhibiting the perceived metallic taste. In those who suffer from intractable phantogeusia, a trial of ice cubes or mechanisms to reduce temperature of the tongue is warranted.