APIK Journal of Internal Medicine

CASE REPORT
Year
: 2020  |  Volume : 8  |  Issue : 2  |  Page : 85--87

A rare case of movement disorder disease


R Madhumathi, GN Devamsh 
 Department of Medicine, Bengaluru Medical College and Research Institute, Bengaluru, Karnataka, India

Correspondence Address:
Dr. G N Devamsh
Department of Medicine, Victoria Hospital, Bengaluru Medical College and Research Institute, K R Market, Bengaluru - 560 002, Karnataka
India

Abstract

Hemifacial spasm (HFS) is a neuromuscular disorder characterized by brief or persistent involuntary tonic or clonic contractions of the muscles innervated by the ipsilateral seventh cranial nerve. It may be idiopathic or secondary to an identifiable cause. It is most frequently attributed to vascular loop compression at the root exit zone of the facial nerve. However, there are several other causes of HFS. Here, we report a case in whom HFS was a presenting feature of central nervous system (CNS) toxoplasmosis. A 53-year-old, known diabetic with retroviral disease on highly active antiretroviral therapy presented with a 6-day history of involuntary, episodic twitching of the left side of his face. There were no associated symptoms. The patient was afebrile, and there was no lymphadenopathy. Examination revealed left HFS. The rest of the neurological examination was normal. Hemogram, liver function test, renal function test, and serum electrolytes were normal. Hepatitis B, C and syphilis serology were negative. CSF showed three lymphocytes, normal protein, and low glucose. Chronic meningitis workup was negative. Magnetic resonance imaging with contrast showed multiple focal ill-defined T2/fluid-attenuated inversion recovery hyperintensities with rim-like enhancement, likely infective. There was no evidence of bony/vascular abnormalities. Toxoplasma serology was positive. The patient recovered with treatment for CNS toxoplasmosis. The prevalence and pathophysiology of HFS have not been widely researched upon. Our patient's HFS was due to CNS toxoplasmosis. Many patients go undiagnosed. Infections such as otitis media, neurocysticercosis, and CNS tuberculosis have been reported to cause HFS. Ours is the first case report attributing CNS toxoplasmosis as the etiology for HFS. The most probable explanation in our case would be irritation/compression of the facial nerve root along its intracranial course due to a focal inflammatory process.



How to cite this article:
Madhumathi R, Devamsh G N. A rare case of movement disorder disease.APIK J Int Med 2020;8:85-87


How to cite this URL:
Madhumathi R, Devamsh G N. A rare case of movement disorder disease. APIK J Int Med [serial online] 2020 [cited 2020 Aug 13 ];8:85-87
Available from: http://www.ajim.in/text.asp?2020/8/2/85/282846


Full Text



 Introduction



Hemifacial spasm (HFS) is a neuromuscular disorder characterized by brief or persistent involuntary tonic or clonic contractions of the muscles innervated by the ipsilateral seventh cranial nerve. It usually starts as a tonic contraction of the lower eyelid followed by involvement of the periorbital, facial, and perioral muscles. The spasms may be aggravated by psychological stress or speaking.[1] It may result in mild progressive facial weakness if untreated. HFS is rarely bilateral. It may be primary (idiopathic) or secondary to an identifiable cause. A mechanical compression of the facial nerve exit zone at the brainstem has been postulated as the major cause of HFS. It is most frequently attributed to vascular loop compression at the root exit zone of the facial nerve. However, there are several other causes of HFS.[2] Here, we report a case in whom HFS was a presenting feature of central nervous system (CNS) toxoplasmosis.

 Case Report



A 53-year-old gentleman, known case of diabetes and retroviral disease on abacavir + lamivudine + efavirenz regimen treated for pulmonary and abdominal tuberculosis 2 years back and declared cured presented with a 6-day history of involuntary, episodic twitching of the left side of his face [Figure 1]. Each episode lasts up to 3–5 min without interruption and subsides spontaneously. These episodes were occasionally precipitated by stress. There were no associated symptoms. It is limited to the left side and does not persist during sleep.{Figure 1}

On examination, the patient was afebrile, and there was no lymphadenopathy. Examination revealed constant irregular contractions of the right orbicularis oris, orbicularis oculi, and platysma. Examination of cranial nerves was normal. The rest of the neurological examination was normal.

Investigations

Hemogram was normal. Erythrocyte sedimentation rate was 55 mm/h. Liver function test, renal function test, and serum electrolytes were normal. Hepatitis B, C and syphilis serology were negative. CSF showed three cells (lymphocytes) with normal protein and low glucose (28 mg/dl) levels. Chronic meningitis workup was negative. Contrast-enhanced computed tomography brain from the base of the skull employing 5-mm sections showed an ill-defined hypodense area in right parietal lobe convexity with surrounding focal meningitis, likely infective etiology. Magnetic resonance imaging with contrast showed focal ill-defined T2/fluid-attenuated inversion recovery hyperintensities with rim enhancement in the right frontal lobe, left basifrontal lobe, left insula, and right occipital lobe, likely infective [Figure 2]. There was no evidence of bony/vascular abnormalities. Magnetic resonance spectroscopy showed mildly increased Cho/NAA (1.4) and reduced NAA/Cr (1.1) ratio with increased lipid lactate peak. Toxoplasma serology was positive.{Figure 2}

Course in hospital

The patient stayed in the hospital for 21 days during which the patient was treated with antiretroviral therapy. Carbamazepine was started for hemifacial spasm. After investigations, the patient was started on pyrimethamine and sulfadiazine for toxoplasmosis and discharged. The patient on follow-up had complete resolution of his symptoms.

 Discussion



The prevalence and pathophysiology of HFS have not been widely researched upon. Our patient presented with HFS and was found to have CNS toxoplasmosis. Although several cases of HFSs are due to vascular abnormalities, tumors, or injury to the facial nerve, many patients go undiagnosed. Infections such as otitis media, neurocysticercosis, and CNS tuberculosis have been reported as etiologies for HFS.[3],[4] Ours is the first case report attributing CNS toxoplasmosis as the etiology for HFS. The most probable explanation for HFS in our case would be irritation/compression of the facial nerve root along its intracranial course due to a focal inflammatory process.

This case report highlights the possibility of alternate diagnosis in patients presenting with HFS and the requirement for detailed clinical history, examination, and laboratory/imaging studies to identify the cause of HFS.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Paul BW, Joseph MC, Jose B. Localization in clinical neurology. Lippincott Williams and Wilkins publishers, 2011;6:435-49.
2Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. Harrison's Principles of Internal Medicine. New York: McGraw-Hill Professional Publishing; 2015;19:2124-5.
3Yaltho TC, Jankovic J. The many faces of hemifacial spasm: Differential diagnosis of unilateral facial spasms. Movement Disorders, 2011;26:1582-92. doi:10.1002/mds.23692.
4Sandyk R. Hemifacial spasm in tuberculous meningitis. Postgraduate medical journal, 1983;59:570-1.