ABSTRACT
Feeling of body ownership is a complex process with different brain mechanisms involved in integrating the varied and multiple representations of the body . The ability to discriminate between one's own and others' body parts can be lost after brain damage. We report a unique case study of a patient with head injury who experienced a phenomenon where he felt that his head was positioned with another person standing next to him. We describe this as a form of pathological embodiment and call it the "head mislocalization" phenomenon. We report his clinical findings and using the methods of lesion mapping and lesion network mapping postulate the neural mechanisms for this symptom.
Subject(s)
Brain Injuries, Traumatic , Humans , Male , Brain Injuries, Traumatic/complications , Brain Injuries, Traumatic/pathology , Body Image , Perceptual Disorders/etiology , Perceptual Disorders/physiopathology , AdultABSTRACT
BACKGROUND: Mercury is a naturally occurring heavy metal that finds wide application in industrial and household settings. It exists in three chemical forms which include elemental (Hg0 ), inorganic mercurous (Hg+) or mercuric (Hg++) salts, and organic compounds. All forms are highly toxic, particularly to the nervous, gastrointestinal, and renal systems. Common circumstances of exposure include recreational substance use, suicide or homicide attempts, occupational hazards, traditional medicines, and endemic food ingestions as witnessed in the public health disasters in Minamata Bay, Japan and in Iraq. Poisoning can result in death or long-term disabilities. Clinical manifestations vary with chemical form, dose, rate, and route of exposure. AIMS AND OBJECTIVES: To summarize the incidence of mercury poisoning encountered at an Indian Poison Center and use three cases to highlight the marked variations observed in clinical manifestations and long-term outcomes among poisoned patients based on differences in chemical forms and routes of exposure to mercury. MATERIALS AND METHODS: A structured retrospective review of the enquiry-database of the Poison Information Center and medical records of patients admitted between August 2019 and August 2021 in a tertiary care referral center was performed. All patients with reported exposure to mercury were identified. We analyzed clinical data and laboratory investigations which included heavy metal (arsenic, mercury, and lead) estimation in whole blood and urine samples. Additionally, selected patients were screened for serum voltage-gated potassium ion channels (VGKC)- contactin-associated protein-like 2 (CASPR2) antibodies. Three cases with a classical presentation were selected for detailed case description. RESULTS: Twenty-two cases were identified between August 2019 and August 2021. Twenty (91%) were acute exposures while two (9%) were chronic. Of these, three representative cases have been discussed in detail. Case 1 is a 3.5-year-old girl who was ought to the emergency department with suspected elemental-mercury ingestion after biting a thermometer. Clinical examination was unremarkable. Chest and abdominal radiography revealed radiodense material in the stomach. Subsequent serial radiographs documented distal intestinal transit of the radiodense material. The child remained asymptomatic. This case exemplifies the largely nontoxic nature of elemental mercury ingestion as it is usually not absorbed from the gastrointestinal tract. Case 2 is a 27-year-old lady who presented with multiple linear nodules over both upper limbs after receiving a red intravenous injection for anemia. Imaging revealed metallic-density deposits in viscera and bones. Nodular biopsy was suggestive of mercury granulomas. A 24-hour urine mercury levels were elevated. She was advised chelation therapy with oral dimercaptosuccinic acid (DMSA). Case 3 is a 22-year-old lady who presented with acrodynia, neuromyotonia, tremulousness, postural giddiness, tachycardia, and hypertension for 2 months, associated with intractable, diffuse burning pain over the buttocks and both lower limbs, 1 month after completing a 3-week course of traditional medications for polycystic ovarian syndrome. A 24-hour urine normetanephrine levels and mercury levels were markedly elevated. Serum anti-VGKC antibodies were present. She was treated with glucocorticoids and oral DMSA with a favorable clinical response. CONCLUSIONS: The clinical manifestations of mercury toxicity are highly variable depending on the source, form, and route of mercury exposure and are related to its toxicokinetics.
Subject(s)
Mercury Poisoning , Mercury , Poisons , Child , Female , Humans , Child, Preschool , Adult , Young Adult , Poison Control Centers , Mercury Poisoning/diagnosis , Mercury/adverse effects , Mercury/pharmacokinetics , Succimer/therapeutic use , Poisons/therapeutic useABSTRACT
INTRODUCTION: Small cortical strokes can mimic weakness of peripheral nerve lesions. However, isolated sensory deficits involving the fingers due to cortical lesions are rare. METHODS: We present a case of a 46 year old man with cerebral venous thrombosis, and a haemorrhage restricted to the postcentral gyrus, who reported numbness in an ulnar neuropathy-like distribution. Testing of somatosensory (SSEP) and pain-related evoked potential (PREP) was done, and the lesion location was mapped to the template brain. RESULTS: The patient had impaired touch and pain but preserved proprioception. He had a normal SSEP response but a prolonged PREP. The lesion was mapped to Broadmann areas 1 and 3b of the postcentral gyrus. DISCUSSION: Sensory cortical representation is such that, the ulnar fingers are medial, and the radial ones are lateral. Also, modality-specific organization is noted with tactile sensation being mapped to areas 1 and 3b, and proprioceptive sensation to area 3a and 2. Thus focal lesions involving the post central gyrus can have selective sensory loss over some fingers and can have selective impairment of some modalities. CONCLUSIONS: We highlight the rare finding of an ulnar-like sensory loss in a patient with cerebral venous thrombosis and the dissociate nature of the sensory loss in isolated cortical lesions.