Left Facial Palsy Research Articles

Demencia talámica por infarto talámico izquierdo y en rodilla de cápsula interna derecha

Thalamic dementia is the clinical consequence of a disorder of both thalami. It is generally secondary to bilateral paramedial thalamic infarcts due to disorders of small blood vessels or cardioembolism. We report a case of dementia of acute onset involving the left thalamus and the genum of the right internal capsule. A 33 year old man, HIV positive, category B2, admitted to hospital for tuberculous meningitis presented with the acute onset of somnolence, followed by marked bradypsychism, personality changes, marked disorder of executive explicit memory without associated praxic, gnosic or language disorders. Ocular motility remained normal. There was left central facial paralysis with inverse emotive voluntary dissociation. The other cranial nerves were normal. There was left hemiparesia with extensor plantar reflex. No other alterations. Cerebral MR imaging was compatible with paramedial infarcts of the left thalamus and genum of the right internal capsule. Thalamic dementia generally occurs in bilateral paramedian thalamic disorders. There are cases of disorders of executive memory secondary to infarcts of the genum of the internal capsule due to interruption of the thalamotemporal pathways and a contralateral paramedial thalamic lesion.

Lyme borreliosis as a cause of facial palsy during pregnancy

The medical history of a pregnant woman in whom the initial pattern of complaints suggested hyperemesis gravidarum is described. After about 18 days the patient developed left facial palsy. Repeated tests eventually confirmed the diagnosis of neuroborreliosis. The problems concerning diagnostics, therapy and the possible complications of Lyme borreliosis during gestation are described.

Lyme neuroborreliosis mimics stroke: A case report

Zhang Y, Lafontant G, Bonner FJ Jr. Lyme neuroborreliosis mimics stroke: a case report. Arch Phys Med Rehabil 2000;81:519-21. Lyme neuroborreliosis is diagnostically challenging because of its diverse manifestations. The well-documented neurologic spectrum includes lymphocytic meningitis, cranial neuropathy, and radiculoneuritis in the early disseminated stage; and peripheral neuropathy, chronic encephalomyelitis, and mild encephalopathy in the late persistent stage. This case report describes a 74-year-old man who developed progressive left hemiparesis and facial palsy. The patient was hospitalized to rule out a cerebral vascular accident. The diagnosis of Lyme borreliosis was established with serologic studies. The patient was treated with intravenous ceftriaxone and responded with rapid clinical and functional recovery. Lyme neuroborreliosis presenting as hemiparesis has rarely been reported. Prompt diagnosis and treatment appear to facilitate symptomatic relief and prevent persistent neurologic deficits. © 2000 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

PERIPHERAL AND CENTRAL NERVOUS SYSTEM LYMPHOMA PRESENTING AS MULTIPLE CRANIAL AND PERIPHERAL RADICULONEUROPATHY

A 58 y.o. man was admitted to our hospital because of severe progressive untreatable radicular pain, limb weakness, and cranial nerve palsies. The patient was well until 2 years before, when he developed progressive perineal sensory loss with impotence. Two months later, he complained of pain in the right foot only partially responding to NSAIDs. A lumbosacral MRI showed a spinal stenosis and multiple lumbar discopathy. During the following year he developed right foot and left arm burning paresthesia only responsive to oral opiates, left facial nerve palsy, right foot drop, arm weakness partially responding to oral steroids, and cyclophosphamide. CSF and electrophysiological studies were consistent with an inflammatory multiple radiculoneuropathy while blood tests, bone scintigraphy, and abdominal echography were normal. Four months before admission, he developed right wrist drop, painful dysesthesia in the left hemithorax, and diplopia. On admission, neurologic examination revealed left oculomotor and facial nerve palsies, distal>proximal weakness in the extensor muscles of the right arm, right foot drop, superficial and deep sensory loss on the right leg, and ubiquitary absent deep tendon reflexes. Four additional spinal taps revealed markedly increased proteins with slightly increased cells (always below 10/mm3) but no tumor cell. Nerve conduction studies were consistent with multiple radiculoneuropathy, while sural nerve biopsy showed an axonal neuropathy. Bone marrow biopsy, chest and abdominal CT, and endoscopy of the gastrointestinal tract were negative for neoplastic lesions. A brain and cervical MRI revealed multiple gadolinium enhancing hyperlucencies in the thalamus, caudate nucleus, and spinal cord. The patient was treated with intravenous steroids and IVIg with no response and with opiates for severe pain. One month later, the patient developed deep vein thrombosis treated with anticoagulants followed four days later by a fatal massive intracranial hemorrhage. Autoptic studies revealed a widespread non‐Hodgkin's type B lymphoblastic centrocitic lymphoma involving the stomach, liver, lung, thyroid, spleen, cauda equina, brain, and the spinal cord.This report draws attention to the unusual presentation of a lymphoproliferative disease that escaped an extensive diagnostic evaluation during life.

Acute cerebellar ataxia of a patient with SLE

We described a 28-year-old woman with systemic lupus erythematosus (SLE) presented with digestive tract, skin and renal symptoms and afterwards developed acute cerebellar ataxia, a paresis of the right inferior rectus muscle, left abducens paralysis and left facial palsy which seemed to be consistent with a brainstem lesion visible on magnetic resonance imaging (MRI). This lesion disappeared within 9 days of corticosteroid treatment. It is suggested that this lesion is focal edema induced by acute changes in the blood brain barrier secondary to a vasculopathy. Other causes, including local infarction, are unlikely.

Ｍｅｌｋｅｒｓｓｏｎ‐Ｒｏｓｅｎｔｈａｌ症候群例

We report a case of Melkersson-Rosenthal syndrome. The case involved an eight-year-old girl. She had experienced left facial paralysis and its spontaneous regression two years before she first came to our clinic with left recurrent facial paralysis and lower lip swelling. Evoked electromyography revealed that the ratio between left and right was 5%. Recovery of facial nerve function was observed after administration of a steroid. Six months later, right facial paralysis occurred, but it disappeared after steroid therapy. Three years after her first visit, right facial paralysis recurred. Because lingua plicata was also exhibited, the diagnosis of Melkersson-Rosenthal syndrome was confirmed. Complete recovery from right facial paralysis was observed after steroid therapy. Although her mother had a history of sarcoidosis, the patient's chest roentgenography, serum angiotensin converting enzyme level, and ophthalmological evaluation for uveitis revealed no signs of sarcoidosis.

Crioglobulinemia mixta esencial como causa de accidente cerebrovascular isquémico

Involvement of the central nervous system in patients with essential mixed cryoglobulinaemia is rare, and there are few cases described in the medical literature. Moreover, the mechanism by which lesions are produced in the central nervous system is still not clear. We describe the case of a 35 year old woman who presented with dysarthria, weakness and paraesthesia of her left limbs and left central facial paralysis of sudden onset. Vascular studies showed the presence of IgG-IgM polyclonal positive cryoglobulins and polymerase chain reaction (PCR) showed hepatitis C virus to be present. Cerebral magnetic resonance showed ischemic lesions in the tail of the right caudate nucleus and right corona radiata and the posteromedial part of the right putamen. Other investigations were negative or normal. In young patients with cerebral vascular pathology the possibility of hepatitis C and essential mixed cryoglobulinemia should be considered, especially when the transaminases are raised as in our patient. We consider that the physiopathological mechanisms must be related to factors which determine a prothrombotic state in the arterial bed involved.

Sudden unexpected death following stellate ganglion block

A 29-year-old woman, who had been suffering from left facial palsy, died 3.5 hours after undergoing stellate ganglion block (SGB). Autopsy revealed subcutaneous emphysema of the body, bilateral pneumothorax and a huge post-tracheal hematoma. The lower half of the trachea was markedly flattened by pressure from this hematoma. The cause of death was certified as airway obstruction due to a post-tracheal hematoma following SGB. The doctor cut both the anterior and the posterior wall of the trachea, because the trachea was flattened by the hematoma. He then intubated and sent air into the post-tracheal space. We consider that the patient could have recovered if she had received the correct tracheotomy. We therefore conclude that there was professional error on the part of the doctor in the form of medical malpractice.

Physical Therapy for Facial Paralysis: A Tailored Treatment Approach

Bell palsy is an acute facial paralysis of unknown etiology. Although recovery from Bell palsy is expected without intervention, clinical experience suggests that recovery is often incomplete. This case report describes a classification system used to guide treatment and to monitor recovery of an individual with facial paralysis. The patient was a 71-year-old woman with complete left facial paralysis secondary to Bell palsy. Signs and symptoms were assessed using a standardized measure of facial impairment (Facial Grading System [FGS]) and questions regarding functional limitations. A treatment-based category was assigned based on signs and symptoms. Rehabilitation involved muscle re-education exercises tailored to the treatment-based category. In 14 physical therapy sessions over 13 months, the patient had improved facial impairments (initial FGS score= 17/100, final FGS score= 68/100) and no reported functional limitations. Recovery from Bell palsy can be a complicated and lengthy process. The use of a classification system may help simplify the rehabilitation process.

Diaphragmatic paralysis due to Lyme disease

Lyme disease is a tick-borne spirochaete infection which, in a proportion of patients, can lead to neuropathy. This article describes a case of diaphragmatic paralysis due to Lyme disease. A 39-yr-old male presented to the hospital because of an acute left facial palsy. Six weeks prior to admission he had developed a circular rash on his left flank during a camping holiday. He also complained of shortness of breath and arthralgia for 1 week. His chest radiograph demonstrated a raised right hemi-diaphragm. Diaphragmatic paralysis was confirmed by fluoroscopy (a positive sniff test). Serology revealed evidence of recent infection by Borrelia burgdorferi. On the basis of the patient's clinical presentation, a recent history of erythema migrans, and positive Lyme serology, a diagnosis of neuroborreliosis was made. He received oral doxycycline therapy (200 mg x day(-1)) for three weeks. Facial and diaphragmatic palsies resolved within eight weeks. On the basis of this case, a diagnosis of Lyme disease should be considered in patients from endemic regions with otherwise unexplained phrenic nerve palsy.

An Autopsy Case of Wegener''s Granulomatosis with Pachymeningitis

A 61-year-old woman presented with high fever, headache and left facial palsy with diplopia. Histopathological examination of the biopsied specimens taken from nasal mucosa and kidney revealed a granulomatous angiitis with giant cell infiltration. Ga-DTPA-enhanced magnetic resonance imaging (MRI) revealed a thickening of dura mater in the middle cranial fossa and tentorium cerebelli. The observed left facial and occulomotor palsy was considered to be caused by pachymeningitis associated with Wegener's granulomatosis (WG). Cyclophosphamide combined with prednisolone effectively improved the symptoms. However, the patient died of acute interstitial pneumonitis, presumably caused by cyclophosphamide. The pathohistology obtained in the autopsy revealed a fibrous thickening of the dura mater in the left meningen with a segmental scarring of the arteries and a necrotizing arteritis in the kidney.

耳科的諸症状を呈した急性骨髄性白血病例

A case of a 19 year-old male with acute myelocytic leukemia (AML) is reported. The patient visited us because of left facial nerve palsy and acute otitis media on both sides. He was diagnosed as AML on the basis of blood and bone marrow examinations. These symptoms subsided after chemotherapy. Two months later, however, the patient's left facial nerve palsy recurred and a granular mass was observed in his right external ear canal. At that time, results of a blood examination were normal. This mass was excised for histopathological examination, and the presense of leukemic cells was proven. This patient underwent chemotherapy again, in addition to radiotherapy but died because of general deterioration of his condition.In this case, histopathological examination was instructive.

中耳結核を伴う上咽頭結核例

A case of epipharyngeal tuberculosis with middle ear tuberculosis is reported. A 4lyear-old female complained of left otorrhea and left facial nerve palsy. Examination of the epipharynx revealed a granular mass. A biopsy from the epipharynx showed only inflammatory changes. A smear of ear discharge and post nasal discharge showed no positive results. To facilitate diagnosis and to reduce the inflammation, we performed an exploratory tympanotomy and biopsy of the epipharynx under general anesthesia. The pathological findings were consistent with Mycobacterium tuberculosis infection. Anti-tuberculosis chemotherapy was performed for one year and the epipharynx granuloma disappeared and the facial nerve palsy was reduced. The present case suggests that it can be difficult to diagnose tuberculosis and that it is very important to consider tuberculosis in cases of intractable inflammation of the head and neck region.

一側突発難聴で発症した髄膜癌腫症例

Meningeal carcinomatosis is caused by diffuse metastasis from solid malignant tumors to the leptomeninges. In this article we report a case of meningeal carcinomatosis, which initially presented as unilateral sudden profound hearing loss and was finally diagnosed by cerebrospinal fluid cytology.A 42-year-old woman with a history of breast cancer was seen at our hospital complaining of dizziness and tinnitus in her left ear. Six days later, she suffered left sudden hearing loss, and left facial palsy was seen two weeks later. No tumor was evident on either magnetic resonance imaging or computed tomography. One month later, diplopia and severe headache appeared and she was diagnosed with meningeal carcinomatosis by cerebrospinal fluid cytology.Consideration of the possibility of meningeal carcinomatosis is necessary when diagnosing sudden profound hearing loss in a patient with a history of the malignant tumor.

Facial nerve neurinoma in a child

Facial nerve neurinoma is a benign tumor, infrequent and exceptional in children. It's clinical manifestation depends on it's location and extension, facial palsy being its most frequent sign. Complementary examinations, namely image-diagnosis studies and audiometric tests become essential. Certain diagnosis is made by pathological anatomy. The reported case is a 13-year-old patient suffering from left peripheral facial palsy with an evolution of 8 months who went through a middle cerebral fossa and transmastoid combined tract.

耳下腺原発癌肉腫の２症例

Two rare cases of carcinosarcoma of the parotid gland are reported. Case 1: A 74-year-old male complaining of swelling in the right parotid region and right facial palsy was admitted to our hospital. He underwent resection of the salivary gland, which was found to contain a malignant tumor (T4bN0M0). He later underwent postoperative radiation therapy (60 Gy). The patient is still alive 7 months after the operation. Case 2: A 57-year-old male complaining of swelling in the left parotid region and left facial palsy was admitted to our hospital. He also underwent resection of a malignant tumor of the salivary gland (T4bN1M0) and postoperative radiation therapy. He is still alive 6 months after the operation. Histologically, the tumors in both cases revealed typical features of carcinosarcoma, consisting of epithelial and non-epithelial histologic components; namely, undifferentiated carcinoma and malignant fibrous histiocytosis. In the literature, carcinosarcoma has been reported to be very malignant due to its large incidence of local recurrence, suggesting that for this tumor, extensive surgical resection is necessary.

Cephalic Tetanus in a Nontraumatized Patient with Left Facial Palsy

Cephalic Tetanus in a Nontraumatized Patient with Left Facial Palsy

Parotid lymphangioma. A case report

Parotid lymphangiomas occur rarely in childhood, and they are usually detected in infancy or early childhood. They grow slowly and present as painless, soft fluctuant masses. Rapid enlargement of the mass is usually associated with trauma, infection or hemorrhage into the cysts, and enlargement can lead to severe complications due to mass effect such as tracheal or esophageal compression and facial weakness. We report a case of parotid lymphangioma with clinical presentation of a rapidly enlarging mass in the left parotid region and facial palsy after aspiration of the mass at the age of 10 years. The facial weakness resolved completely when the size of mass decreased spontaneously.

A Case of Uveitis Associated with Chronic Active Epstein-Barr Virus Infection

Ocular complications of chronic active Epstein-Barr virus infection (CAEBV) have rarely been reported. We describe a 7-year-old girl with CAEBV with associated uveitis. The patient was first observed to have recurrent fever and hepatosplenomegaly in August 1991. She presented with left facial nerve palsy in June 1993. Ocular examination showed right iridocyclitis. Both optic disks were swollen, and the retinal vessels were dilated. Antibody titers to EBV were markedly elevated. Treatment with topical steroids. systemic interleukin-2 and splenectomy dramatically relieved all her symptoms. including the ocular ones.

耳下腺内顔面神経鞘腫の２症例

Two cases of intraparotid facial nerve schwannoma are presented. Case 1 was a 38-year-old female who complained of a slowly growing tumor under her left ear. She had had an open biopsy at another hospital about two years earlier ; the tumor was diagnosed histologically as schwannoma. Surgical excision was performed, and the tumor was diagnosed as a schwannoma originating from the buccal branch of the facial nerve. Case 2 was a 74-year-old female who complained of a slowly growing tumor under her left ear. The tumor was accompanied by slight pain, and left facial palsy was noted. Surgical excision was performed under a preoperative diagnosis of malignant parotid gland tumor. However, the tumor was found to be a schwannoma originating from the main trunk of the facial nerve, the upper part of the tumor was growing into the stylomastoid foramen.Intraparotid facial nerve schwannoma is rare, and in Japan, only 26 cases have been reported to date.