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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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- Journal:
- 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 The delusion that their body has been replaced by a purely inanimate azooic (but physical entity), such as a robot or a droid, has not hitherto been described.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 When confronted with commitment papers signed by her father, she denied their truthfulness, insisting that he had been replaced by an imposter.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 Over time, she expressed the belief that she had been replaced by another person, whom she refused to identify. The following day she refused all food and water proclaiming that she had died and been replaced by a machine revealing, “I am not her.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 Upon presentation, she exhibited Capgras syndrome, the delusional belief that a familiar person has been replaced by a double.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
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
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.
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.
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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- Journal:
- CNS Spectrums / Volume 24 / Issue 1 / February 2019
- Published online by Cambridge University Press:
- 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.
74 Alpha Lipoic Acid Responsive Hypergeusia
- Sarah E. Cormie, 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. 212-213
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Introduction
Improvement in hypergeusia in response to alpha lipoic acid treatment has not heretofore been described. Such a case is presented.
MethodsCase Study: A 64 year old right handed nasute female noted the sudden onset of salty hypergeusia, about 200% saltier than foods should be. Concurrently she experienced a constant phantogeusia of salt involving the front half of her tongue, lips, and inside her mouth. She denied any smell problems, cacogeusia, or palinageusia. This persisted for five months until treatment with 1800mg/day of alpha lipoic acid, whereupon, over a one month duration, the salty hypergeusia gradually resolved. Suppression of the salty hypergeusia continued until she developed an upper respiratory infection, whereupon, despite the continuation of alpha lipoic acid, the salty hypergeusia returned to 250% of normal. During the cold, her ability to taste dropped down from 100% to 80%, and ability to smell dropped from 100% to 50% and upon resolution of the cold, the senses returned to normal and the salty hypergeusia remitted.
ResultsAbnormalities in Neurologic Examination: Reflexes: 3+ bilateral quadriceps femoris and pendular. Chemosensory testing: Olfaction: Alcohol Sniff Test: 12 (hyposmia), Phenylethyl Alcohol Threshold: greater than –2 (anosmia). Suprathreshold Amyl Acetate Odor Intensity Testing: parallel pattern (normosmia). Pocket Smell Test: 4(normosmia). Retronasal Olfactory Testing: Retronasal Smell Index: 8(normosmia). Gustatory testing: Propylthiouracil Disc Taste Test: 5(normogeusia). Taste Super threshold Testing: normogeusia to sodium chloride, sucrose, and phenylthiocarbamol: hypogeusia(10–30%) to urea; ageusia(0%) to hydrochloric acid. Taste Quadrant Testing: taste weakness to sodium chloride for the entire mouth.
DiscussionThe alpha lipoic acid may have acted to improve smell and associated enhanced retro nasal smell, inhibiting savory gustatory discharge, and thus, effectively reducing salt perception. Such a mechanism would also explain the recurrence of hypergeusia with the upper respiratory infection; the infection presumably transiently reducing the olfactory ability, overcoming any olfactory enhancing effects of alpha lipoic acid. On the other hand, this agent could have acted to improve smell as well as taste. With such enhanced chemosensory capacity, the normal olfactory and gustatory components of food would have inhibited competing pathologically discharging gustatory receptors for salt, reducing dysgeusia and hypergeusia. Moreover, the alpha lipoic acidmay have acted to focus the patient’s attention on the gustatory stimulation which may have caused her to perceive not just the predominant salt sensation but enhanced perception of the other gustatory sensations which acted to competitively inhibit the perception of salt. Further investigation of alpha lipoic acid in the management of dysgeusia and hypergeusia is warranted.
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
40 Pseudo Cranial Nerve I Dysfunction: Subjective Hyposmia and Subjective Hypogeusia but Normosmia and Normogeusia - 3 cases
- Kristal Benskin, 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. 196-197
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INTRODUCTION
Hyposmia refers to reduced ability to smell and hypogeusia is a partial loss of the ability to taste (Hummel, Basile, & Huttenbrink, 2016). Complaints of hyposmia and hypogeusia in the presence of normosmia and normogeusia has not heretofore been described. Three such cases are presented.
OBJECTIVETo explore the complaints of reduced smell and taste with normal objective olfaction and gustation.
METHODAll patients were given screening tests for smell and taste and obtained scores consistent with normosmia and normogeusia. The 12-item version of the Brief Smell Identification Test (B-SIT), using the odorants banana, chocolate, cinnamon, gasoline, lemon, onion, paint thinner, pineapple, rose, soap, smoke and turpentine was used. The Retronasal Olfactory Test was used to determine their perception of flavour and the Proplythiouracil Disc Taste Test used for gustation. Each patient also underwent a complete physical and neurological examination with any abnormalities mentioned.
RESULTSCase 1: This 53 year old female, 8months prior to presentation, developed the flu followed by the inability to taste any foods and differentiate between smells, with everything smelling bitter.
Results: Chemosensory testing: Olfaction: Brief Smell Identification Test (B-SIT): 10 (normosmia). Retronasal Olfactory Test: Retronasal Smell Index: 9 (normal). Gustation: Propylthiouracil Disc Taste Test: 7 (normal).
Case 2: This 86 year old female, 6months prior to presentation, developed reduced taste, of gradual onset, to the point upon presentation was only 10% normal. She was able to taste lemons but very little else.
Results: B-SIT: 9 (normosmia). Retronasal Smell Index: 10 (normal). Propylthiouracil Disc Taste Test: 10 (normogeusia).
Case 3: This 63 year old female was nasute until 3months prior to presentation, when she developed an upper respiratory infection, followed by loss of smell and taste to 20% of normal.
Results: B-SIT: 10 (normosmia). Retronasal Smell Index: 7 (normal). Propylthiouracil Disc Taste Test: 10 (normogeusia).
CONCLUSIONDiscordance between subjective and objective findings may be due to the wide distribution of normal in the general population in olfactory ability. The associated reduction in retronasal smell may then be interpreted by the patient as reduced ability to taste. Alternatively, complaints of hyposmia and hypogeusiamay be due to a non-organic need such as malingering or psychosomatic illness, or could represent a primary defect in the cortical integration of smell and taste, interpreted as reduction in perceived flavor, yet the primary sensory neurons and threshold as tested would appear to be normal. This disparity possibly indicates that the testing modalities are too insensitive to demonstrate more subtle sensory perception findings, and suggests the need for more refined testing methods for smell and taste.
43 Tinnitus as an Aura for Sleep Paralysis
- Luvleen Shergill, Jasir Nayati, Reshma Nair, 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. 199
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Objective
To understand that tinnitus may be an aura for sleep paralysis.
BackgroundSleep paralysis is a transient-paralysis which occurs during awakening or falling asleep (Wilson, 1928). Those affected experience symptoms including visual, auditory, and haptic hallucinations, voluntary motor paralysis with intact ocular and respiratory motor movements, and diffuse or localized paresthesias. Sleep paralysis associated with tinnitus as an aura, has not heretofore been described.
MethodsA 34 year-old, right-handed female presented with a 13 year history of sleep paralysis. One month prior, she began to notice tinnitus prior to the onset of sleep paralysis. The tinnitus was bilateral, high-pitched, with a volume intensity of 5/10, lasting seven seconds prior to sleep initiation. She denied hearing loss, vertigo, dizziness, cataplexy, deja vu and jamais vu. After termination of tinnitus, she experienced paresthesia, “like at a dentist’s office” radiating from her posterior neck, to her tongue and down to her toes. She described seeing a white-shadowy male figure moving around her room, lasting seven seconds. Accompanied by a masculine “ahh” sound, lasting for three seconds. The sleep paralysis occurred after these events, lasting up to eight hours, or until her husband wakes her.
ResultsAbnormalities in Physical Examination: General Examination: right arm hemangioma 4 by 5cm. Reflexes: absent bilateral brachioradialis, 1+ bilateral quadriceps femoris and bilateral Achilles tendon. Neuropsychiatric Examination: Calibrated Finger Rub Auditory Screening Test: faint 70 AU (normal).
DiscussionTinnitus has been described as an aura for migraines (Schankin, 2014), temporal lobe epilepsy (TLE) (Florindo, 2006), and narcolepsy-cataplexy (Marco, 1978). These epochs may represent amigranous migraines, which initially present with tinnitus that occurs both during the day and night, forcing the patient to be partially awoken at night with induction of the sleep paralysis sequence. It would be worthwhile to query those with narcolepsy or sleep paralysis if tinnitus precedes the event.
193 A New Syndrome: Phantogeusia-Induced Phantosmia
- Umar Ahmad, 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. 110
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Case Objective
While phantosmia-induced phantogeusia has been described (Ahmed, 20173), the reverse, phantogeusia-induced phantosmia, has not heretofore been described. Such a case is presented.
MethodsCase Study: A 39-yr-old left-handed (pathological) male, six years prior to presentation, noted a sudden onset of phantogeusia of roast cooking, pizza, fruit, strawberries, or a sour taste, and shortly thereafter he would develop unpleasant phantosmias which would sometimes combine with the ambient aroma. These would occur 3-10 times per week and would last for the duration of the phantogeusia, for as long as 1-2 hours. Occasionally the phantosmia would occur first and then induce the phantogeusia of asour taste.
ResultsAbnormalities in Neurologic examination: Mental status examination: Immediate recall: Digit span: 6 digits forward and 3 digits backwards. CN XI, X: Decreased gag bilaterally. Motor Examination: Drift: left pronator drift with right abductor digiti minimi sign and right cerebellar spooning. Gait Examination: Tandem Gait: unstable. Cerebellar Examination: Holmes Rebound Phenomena: bilaterally positive, left greater than the right. Sensory Examination: Ipswich Touch Test: decreased in left lower extremity. Temperature: decreased in left lower extremity. Rydel-Seiffer Vibratory Test: bilateral upper extremities 5, bilateral lower extremities 3. Reflexes: upper extremities 1+, absent lower extremities. Neuropsychiatric Examination: Go-No-Go Test: 6/6 (normal). Animal Fluency Test: 15 (normal). Clock Drawing Test: 3 (abnormal). Center for Neurologic Study Lability Scale: 16 (Pseudobulbar affect).
ConclusionClose connection of the tertiary smell and taste integration areas, where smell and taste converge, in the posterior orbitofrontal cortex, anterior to the insular taste cortex, and posterior to the granular orbitofrontal cortex may have allowed activation of memory engrams connecting these two (Rolls, 19944). Alternatively, electrical discharge from the primary taste area may have spread to involve the cortical representation of smell. Since the cortical area involved in the interpretation and hedonics of taste co-localize with the area involving olfactory hedonics, spread from one area to the other area may occur. As a result of electrical discharge (from an epileptiform focus) or as a result of well-connected and developed memory engrams with associated hedonics, phantom tastes may induce phantom smells. Alternatively, this may represent a distorted retronasal smell whereby the olfactory component of the gustatory hallucination causes a discharge of the olfactory epithelium (a pseudoretronasal smell).
Given the above, treatment of those with both phantosmia and phantogeusia may respond to treatment of phantogeusia alone. Under this construct, the phantosmia is the slave of the phantogeusia whereby management of the taste hallucination will thus eliminate the smell hallucination.
Funding AcknowledgementsSmell and 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
125 Short Duration Monoballismus
- Davinder Dhillon, 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. 79-80
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Study Objective
While monoballismus has been reported to be associated with hemorrhagic lesions in the subthalamic nucleus (Ohnishi, 2009) and multiple sclerosis (MS) (Rosa, 2011), the duration has been reported to be at least six days (Soysal, 2012). A patient with epochs of monoballismus lasting for 45 minutes is presented.
MethodsCase Study: A 57 year old right handed female with attention deficit hereditary disorder predominantly inattentive on amphetamine sulphate, presented with two years of memory loss. For instance, after ordering food in restaurants, by the time the food arrives, she could not recall what she ordered. At the onset of this symptom, she noted three epochs of her left arm jerking for 45 minutes. The jerking would begin with low amplitude and low frequency and rapidly progress to the forearm and arm of greater magnitude and low frequency. With her right hand she would try to hold down her left arm without success. There was no associated paresis, sensory phenomena, headaches, dizziness, presyncope, loss of consciousness, or strong emotions. She admitted to frequent jamais vu.
ResultsAbnormalities: Neurological Examination: Mental Status Examination: Memory: Immediate Recall: 5 digits forward and 2 digits backwards. Cranial Nerve (CN) Examination: CN I: Alcohol Sniff Test 8 (hyposmia). CN XII: tongue tremor on protrusion. Motor Examination: Drift Test: positive right pronator drift. Gait Examination: Tandem Gait: unstable. Reflexes: 0-1 throughout. Neuropsychiatric Examination: Go-No-Go Test: 6/6 (normal). Animal Fluency Test: 15 (normal). Clock Drawing Test: 3 (abnormal). Center for Neurologic Study Lability Scale: 16 (pseudobulbar affect). Other: MRI with and without infusion: normal.
ConclusionTransient tonic-clonic movements of one limb have been described with focal epilepsy associated with diabetic non-ketotic hyperglycemia (Grant, 1985). A metabolic abnormality such as transient hypoglycemia or hyperkalemia can cause a focal dystonia (Soysal, 2012), which theoretically could manifest with monoballismus. This could be a somatic manifestation of underlying conflict, conversion disorder, or as a result of a physical manifestation of panic attack with hyperventilation and tetany (Mihai, 2008). This may be the first manifestation of a generalized cerebral disorder associated with chorea or ballismus such as Wilson’s disease, or Huntington’s Chorea (Mihai, 2008). It is possible that this is a variant of Alien Hand Syndrome with parietal lobe involvement (Shrestha, 2015). But this is unlikely given the absence of hemineglect or hemiagnosia. It is possible that amphetamines may have induced a monochorea. Chronic amphetamine use has been demonstrated to cause chorea (Klawans, 1974) and it theoretically could have caused ballismus movements in this case. In patients who present with short duration monoballismus, evaluation for subthalamic nuclei function, seizure disorders and other origins of ballismus are warranted.
Funding AcknowledgementsSmell & Taste Treatment and Research Foundation
188 Buspirone-Induced Somnambulism
- Sulekho Egal, 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. 107-108
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Objective
Buspirone has not heretofore been reported to trigger somnambulism. Such a case is described.
BackgroundBuspirone is a partial 5HT1A agonist, which acts to suppress REM sleep and increase sleep fragmentation (Ware, 1994).
Design/MethodsA 36-year old right handed woman presented with one-year of constant anxiety and panic attacks with epochs of dyspnea, tachycardia, diaphoresis,paresthesias of both hands, and out of body sensations. She affirmed déjà vu and PM insomnia, and vivid dreams. When in high school she had one sleepwalking event, without recurrence. The patient was begun on buspirone, initially 2.5 mg and raised to 5 mg QHS. Within a day of increasing the dose, she experienced an episode whereby in the early hours in the morning, she removed her pajamas, folded them neatly into a stack next to the bed, and returned to bed, sans clothes. She was amnestic for this event, but based this history on her husband’s report. She discontinued the buspironeand for over 1 year, there has been no recurrence of such events.
ResultsAbnormalities in her neurological examination: Mental Status
ExaminationAnxious. Memory: immediate recall: 7 digits forwards and 4 digits backwards: Cranial Nerve Examination: Cranial Nerve I: Alcohol Sniff Test: 8 cm (hyposmia), Reflexes: 3+ throughout. Neuropsychiatric testing: Clock Drawing test: 4 (Normal). Animal Fluency test: 20 (normal).
ConclusionsBuspirone induced somnambulism may relate directly to its mechanism of action, as a 5HT1A partial agonist. Since other 5HT1A agonists, to cause noctambulism (Raja2012). Buspirone increases sleep fragmentation (Wilson, 2005), and thus may act to disrupt slow wave sleep, promoting susceptibility to somnambulism. Alternatively, her somnambulism may be a nocturnal variant of Buspirone induced dissociative state (Bystritsky, 2013). Given the above, it is worthwhile to query those who are undergoing therapy with buspirone for the development of somnambulism.
Funding AcknowledgementsNo funding.