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Inability to close mouth and dysphagia caused by pseudobulbar palsy: trial treatment by vibration-induced mastication-like movement

Inability to close mouth and dysphagia caused by pseudobulbar palsy: trial treatment by vibration-induced mastication-like movement:

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Pseudobulbar palsy is a medical condition characterized by the inability to control facial movements (such as chewing and speaking) and caused by a variety of neurological disorders.

Pseudobulbar palsy - Wikipedia

https://en.wikipedia.org › wiki › Pseudobulbar_palsy

Causes

Pseudobulbar palsy is the result of damage of motor fibers traveling from the cerebral cortex to the lower brain stem. This damage might arise in the course of a variety of neurological conditions that involve demyelination and bilateral corticobulbar lesions. Examples include:

• Vascular causes: bilateral hemisphere infarction, CADASIL syndrome
• Progressive supranuclear palsy
• Amyotrophic lateral sclerosis
• Parkinson's disease and related multiple system atrophy
• Various motor neuron diseases, especially those involving demyelination
• Multiple sclerosis and other inflammatory disorders
• High brain stem tumors
• Metabolic causes: osmotic demyelination syndrome^[2]
• Neurological involvement in Behçet's disease
• Brain trauma

Pathophysiology

The proposed mechanism of pseudobulbar palsy points to the disinhibition of the motor neurons controlling laughter and crying, proposing that a reciprocal pathway exists between the cerebellum and the brain stem that adjusts laughter and crying responses, making them appropriate to context.^[3] The pseudobulbar crying could also be induced by stimulation in the region of the subthalamic nucleus of the brain.^[4]

Signs and symptoms

Signs and symptoms of pseudobulbar palsy include:

• Slow and indistinct speech
• Dysphagia (difficulty in swallowing)
• Small, stiff and spastic tongue
• Brisk jaw jerk
• Dysarthria
• Labile affect^[5]
• Gag reflex may be normal, exaggerated or absent
• Examination may reveal upper motor neuron lesion of the limbs

Description

An 84-year-old man suddenly developed dysphagia following repeated transient ischaemic attacks. He could not close his mouth, swallow food, or speak. Dislocation of the jaw, atrophy of the tongue, or gag reflex was not seen, but the snout reflex and jaw jerk were exaggerated, and the patient was able to walk. Radiological findings showed occlusion of the right internal carotid artery, leukoaraiosis and atrophy of anterior operculum. The patient's condition was diagnosed as Foix-Chavany-Marie syndrome, a type of pseudobulbar palsy.1 His mouth was kept half-open due to inability to close mouth. We used a bandage to prevent jaw dislocation and stretch the jaw closing muscles.2 Under nutritional control with gastric fistula, swallowing training was started, but dysphagia did not improve. However, vibration stimulation of the mouth with an electric toothbrush induced mastication-like movement in a reflex manner (video 1). After 2 weeks of reflex movement training, the patient was able to close his mouth voluntarily. However, adding swallowing training to the reflex movement training using an electric toothbrush failed to improve dysphagia. The mastication-like movement was analysed with surface electromyogram (EMG) by placing electrodes on the masseter, suprahyoid (digastricus) and orbicularis oris muscles (figure 1A,B). Voluntary masticatory movements were similar to the vibration-induced movements, but did not lead to swallowing movement.3 Although dysphagia of pseudobulbar palsy is difficult to treat, range of movement exercise of the mandibular joint and stimulation of the trigger point have been reported to be useful for opening the mouth and facilitating swallowing in patients with pseudobulbar palsy.4 Because of relatively abundant muscle spindles in the masseter and temporal muscles, the vibratory stimuli from an electric toothbrush probably trigger the jaw closing reflex and facilitate voluntary mastication.5 Stimulation with an electric toothbrush may be a plausible method for treating dysphagia caused by pseudobulbar palsy.

On admission, he was not able to close his mouth and say any word. By applying an electric toothbrush, mastication-like movement was evoked. After two weeks of training with an electric toothbrush, he became capable of closing his mouth voluntarily. “Clo

Video 1

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Figure 1

Surface EMG recorded after 2 weeks of reflex movement training when the patient became able to close mouth voluntarily and make an explosive voice. Electrodes were placed on bilateral masseter and orbicularis oris muscles, and right digastricus and sternocleidomastoid muscles. (A) During voluntary mastication, grouped discharge at approximately 1 Hz for a duration of 700–800 ms was seen in the masseters. (B) By an electric toothbrush, grouped discharges at approximately 1.2 c/s for a duration of 600–1000 ms appeared in the masseter and digastric muscles. When he held the toothbrush between his teeth, reciprocal activation and inhibition was seen between the digastricus (jaw opening muscle) and masseter (jaw closing muscle) (asterisks).

Learning points

• Inability to close mouth and dysphagia caused by pseudobulbar palsy were treated by vibration using an electric toothbrush.
• Mastication-like movement was induced by an electric toothbrush in a reflex manner, and voluntary mastication was possible after 2-week training.
• The acquired voluntary mastication did not lead to swallowing, but vibration using toothbrush should be tried to overcome the nuisance condition of failure of closing mouth.

Acknowledgments

We appreciate Dr Yasuo Kumagai and Dr Akihiro Numao for their management of this patient in the acute hospital.

References

1. ↵
   1. Vinken PJ, 
   2. Bruyn GW

   1. Bruyn GW, 
   2. Gathier JC

   . The operculum syndrome. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical Neurology, vol. Amsterdam: Elsevier Science BV, 1969: 776–83.

   Google Scholar
2. ↵
   1. Kisner C, 
   2. Colby LA

   . Therapeutic exercise: foundations and techniques. 394. 5th edn. Philadelphia, PA: F.A. Davis Corporation, 2007.

   Google Scholar
3. ↵
   1. Nakamura Y, 
   2. Katakura N

   . Generation of masticatory rhythm in the brainstem. Neurosci Res1995;23:1–19.doi:10.1016/0168-0102(95)90003-9

   CrossRefPubMedWeb of ScienceGoogle Scholar
4. ↵
   1. Kojima C, 
   2. Fujishima I, 
   3. Ohkuma R, et al

   . Jaw opening and swallow triggering method for bilateral-brain-damaged patients: K-point stimulation. Dysphagia2002;17:273–7.doi:10.1007/s00455-002-0062-7

   CrossRefPubMedWeb of ScienceGoogle Scholar
5. ↵
   1. Miles TS, 
   2. Flavel SC, 
   3. Nordstrom MA

   . Stretch reflexes in the human masticatory muscles: a brief review and a new functional role. Hum Mov Sci2004;23:337–49.doi:10.1016/j.humov.2004.08.010

   CrossRefPubMedWeb of ScienceGoogle Scholar

Piperacillin-tazobactam induced bicytopenia in low cumulative treatment doses

Piperacillin-tazobactam induced bicytopenia in low cumulative treatment doses:

We present the case of infected wet gangrene of right foot in the setting of poorly controlled type 2 diabetes in a 71-year-old woman. This patient presented with improved infection condition after intravenous piperacillin–tazobactam (PTZ) 2.25 gm every 6 hours treatment and below knee amputation surgery on day 3. However, neutropenia and thrombocytopenia developed on day 13. We consulted a haematologist and performed a series of examinations. However, no significant findings were noted thereafter. PTZ was suspected to be the most likely cause of neutropenia and thrombocytopenia and was hence terminated on day 14 (cumulative dose of PTZ: 126 g) following stabilisation of the infection condition. A transfusion was performed with two units of single donor platelets on day 14 and treated with intravenous dexamethasone 5 mg every 8 hours from day 14 to 16. Her white blood cell and platelet counts increased on day 15 and continued to recover thereafter.

Acute cerebellar ataxia due to Epstein-Barr virus under administration of an immune checkpoint inhibitor

Acute cerebellar ataxia due to Epstein-Barr virus under administration of an immune checkpoint inhibitor:

A 71-year-old male patient with adenocarcinoma of the lung and contralateral lung metastasis under administration of pembrolizumab had symptoms of cerebellar ataxia. We suspected that the symptoms were immune-related adverse events (irAE), but the patient was subsequently diagnosed as cerebellitis due to Epstein-Barr virus (EBV) infection. After steroid pulse therapy, the symptoms of cerebellar ataxia improved immediately. Immune checkpoint inhibitors (ICI) can induce neurological adverse events and cause acute cerebellar ataxia. Initially, irAEs were suspected in this case. His clinical data suggested that reactivation of the virus had occurred because the ICI affected his immune system. This is the first report of a case of acute cerebellar ataxia due to EBV under administration of an ICI.

Pericardial knock

Pericardial knock:

Description

A 69-year-old woman with a history of systemic lupus erythematosus complicated by recurrent episodes of acute pericarditis was admitted to the hospital with chronic, progressive dyspnoea. Physical examination was notable for a jugular venous pressure (JVP) of 18 cm H2O, with paradoxical rise on inspiration (Kussmaul’s sign). The y descent of the jugular venous waveform was observed to be sharp and deep (Friedreich’s sign). Coinciding with the nadir of the y descent, an extra, early diastolic heart sound was heard over the apex. It occurred just after the second heart sound (S2) and was high-pitched, heard best with the diaphragm of the stethoscope. A digital stethoscope was used to record the heart sounds. Simultaneously, an antique phonocardiograph was used to produce visualisation of the sounds in the form of a phonocardiogram. Combining these results, a video was created for analytic and teaching purposes (video 1). The qualities of the extra sound, including pitch, timing and location, were consistent with that of a pericardial knock. In a patient with a history of recurrent episodes of acute pericarditis, the constellation of elevated JVP, Kussmaul’s sign, Friedreich’s sign, and a pericardial knock led to the diagnosis of constrictive pericarditis. A pericardial knock can be difficult to distinguish from an S3 gallop; it is a high-pitched, diastolic sound heard 0.09 to 0.12 s after the aortic component of S2 (A2).1–3 It tends to be louder, higher-pitched, and slightly closer to A2 than the low-pitched S3 gallop, which occurs 0.1 to 0.2 s after A2.2 3 The sound is presumed to occur when stiff and thickened pericardium cause sudden arrest of ventricular filling during diastole.2 3

bcr2019233546V1

video 1

Learning points

• The pericardial knock is a high-pitched, early diastolic sound that occurs when unyielding pericardium results in sudden arrest of ventricular filling. It can be an important clue to the diagnosis of constrictive pericarditis.2 3
• The pericardial knock occurs earlier in diastole (0.09–0.12 s after the aortic component of the second heart sound (A2)) compared with the S3 gallop (0.1–0.2 s after A2).1–3
• Phonocardiography combined with modern digital recording devices can be used to facilitate the understanding and recognition of extra heart sounds.

References

1. ↵
   1. Wood P

   . Chronic constrictive pericarditis. Am J Cardiol1961;7:48–61.doi:10.1016/0002-9149(61)90422-2

   CrossRefPubMedWeb of ScienceGoogle Scholar
2. ↵
   1. Marriott HJL

   . Bedside cardiac diagnosis. Philadelphia, PA: Lippincott Company, 1993.

   Google Scholar
3. ↵
   1. Tavel ME

   . Clinical phonocardiography and external pulse recording. 2nd edn. Chicago, Illinois: Year Book Medical Publishers, Inc, 1967.

   Google Scholar

Footnotes

• Contributors AMM captured the audio and phonocardiographic tracing of the heart sounds. TEB created the synchronised video. TEB, NNL, GSO, PDS, and AMM were involved in writing the manuscript.