This is case report of Marchiafava Bignami Syndrome in a 36 years old male. Marchiafava Bignami Syndrome is a rare entity with few reports in literature across the world. This syndrome is associated with chronic alcoholism in old and aged alcoholics. The exact etiology is unclear and the clinical course can be mild to a very terrible fatal illness. The only treatment is alcohol abstinence and proper nutrition.
CASE HISTORY
36 years old male had sudden onset giddiness associated with blackouts which started 5-6 years back. He took symptomatic treatment for the same. Recently, six weeks back he noted that he could not walk normally. There was swaying bilaterally but more so on the left side. The relatives at home noted that his gait was altered. He came to our OPD clinic for swaying, impaired gait, dysarthria. On enquiry it was found that he had a long history of
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It is probably caused by the combination of alcohol abuse and malnutrition, leading to metabolic, toxic, and vascular disturbances7. The main pathologic changes seen in MBD include symmetrical demyelination and necrosis of the central part of the corpus callosum, with relative sparing of dorsal and ventral layers. Rarely, other structures of the CNS like optic chiasm and tracts, putamen, anterior commissure, cerebellar peduncles and, cortical gray matter and U fibers may be involved8. Marchiafava-Bignami disease may present in various clinical forms9.
Acute Marchiafava - Bignami disease includes seizures, impairment of consciousness, and rapid death. Subacute Marchiafava - Bignami disease includes variable degrees of mental confusion, dysarthria, behavioural abnormalities, memory deficits, signs of interhemispheric disconnection, and impairment of gait. Chronic Marchiafava - Bignami disease, which is less common, is characterized by mild dementia that is progressive over
F.C. is a 54-year-old man with a history of chronic heavy alcohol use. He has frequent bouts of gastrointestinal bleeding for which he has been hospitalized on six separate occasions over the years. He continues to drink and exhibits most of the common manifestations of alcoholic cirrhosis. He was recently hit by a car and was hospitalized for a broken leg. He appeared to be under the influence of alcohol at the time of the accident and had a blood alcohol level of 0.18. F.C.’s family reports that his mental functioning has deteriorated significantly over the past few months.
The general health of the patient is currently being compromised due to present illness mentioned above, but is stable. L.H. reports his usual health to be, “normal and not too crazy like this”. Patient has some fatigue noted while conducting daily activities; No recent weight change, fever or sweat. The skin noted to some discoloration on upper right side of back. There is no pruritus, rash or lesions present. Bruises noted bilateral on arms. Patient reported taking baby aspirin as daily medication. His hair is greying and thinning with no hair loss.
Patient is a 50-year-old-year-old left-handed white male who presents with his wife for evaluation of multiple symptoms that have been present since an MVA in 02/2013. At that time, he was T. boned and his car was totaled. He has amnesia for the event and is unaware whether or not he hit his head. The airbag did deploy. Afterwards, he was confused and noted significant pain in his neck and upper back. Since then, he has had multiple symptoms. He does have involuntary twitching on the right, more than left, both hands, legs, and sometimes feet. He demonstrates one of these twitches and it looks like a focal myoclonic jerk of a limb. These occur on a daily basis. He also has problems with his left thumb and index finger locking up. When he is fatigued, especially when his neck gets tight, he has some problems with word finding, paraphasic errors, and syntax errors. He did see Anthony P. Knox,
She converses appropriately. Blood pressure 92/60 supine. Blood pressure decreased to 72/50 standing. Pulse is 90 and regular. Weight 113 pounds. She has a normal appearance of her face and does not have a masked appearance of her face. She has good strength throughout her face. She has good strength of her extremities. She has only minimal cogwheel rigidity at the left wrist, but no cogwheel rigidity at the right wrist. She has no tremor of her hands. She moves her extremities freely and with normal speed. She is able to rise on her own from a sitting to a standing position, only minimal bradykinesia of standing. She walks fairly freely and there is a normal cadence of her gait. She did not have dyskinetic movements of her extremities. She is able to walk, including turning without losing her balance. She does not shuffle her feet when walking. She does not have en bloc turning. She has good posture stability
Patient is a 60-year-old Latin American female, who presents with her husband for evaluation of some spells. She seems to have two different things going on. She did report intermittent episodes of feeling of weakness with blurred vision, diffuse paresthesias and a sensation she is about to pass out or the sensation of before undergoing generalized surgery, feeling like she is being sucked down. There is no loss of consciousness with this. She is unable to give any further history, except these events have been going on for about a month. They are almost daily. She does note they happen after eating, at which point, she will fall asleep easily. Otherwise, she denies any loss of consciousness,
Brathen, G., Ben-Menachem, E., Brodtkorb, E., Galvin, R., Garcia-Monco, J., Halasz, P., ... Blackwell, W. (2010, September 6). Alcohol-related seizures
On examination, cervical and lumbar spine is restricted in all planes with increased pain. Muscle guarding is also noted. The patient is not able to heel and toe walk. He is obese and deconditioned. Straight leg raise (SLR) is positive bilaterally. Muscle guarding is noted along cervical paraspinal and trapezius muscle groups bilaterally. Sensation is normal to light touch, pinprick, and temperature along all dermatomes of the bilateral upper extremities, except right C6-8, decreased to
-Contacted Desert Springs facility and follow-up on the patient. Spoke to medtech Muriel and stated that another caregiver has been going to patient’s room and no complaint or concern was raised from the patient. Instructed Muriel to see the patient and she stated that patient is the same and “normal” sitting up in her recliner’s chair. Speech is clear and no facial droop per Muriel. Per Muriel, patient did complaint about a week ago with right foot
Patient is a 58-year-old right-hand white male interviewed in the presence of his wife. He was previously seen by me last month for admission for the acute onset of vertigo with possible TIA or stroke as etiology. He stated that he awoke on 06/18/2015 in his usual state of health and then went to work and while there, he had the sudden onset of marked spinning vertigo. He was unable to walk straight, but denied any bilateral lower extremity weakness. He did have nausea and vomited several times. He initially denied any diplopia, visual field cut, blurred vision, facial asymmetry, facial or body sensory changes, dysarthria, or focal weakness. He continued to have marked vertigo in the emergency room,
What is the most likely causative agent and what type of disease manifestation does this patient have?
Patient is an 86-year-old right-handed white female who is a poor historian. She states she saw me several years ago, but cannot recall for what. She did see Geoffrey Starr, MD in 2011 for episodes of numbness and tingling in the right side of her cheek. He did a workup, which included the EEG, EMG, and carotid studies. She was complaining of some right upper extremity and left lower extremity numbness and tingling as well. These were all negative. Her PCP switched her from aspirin 81 mg to Plavix 75 mg. Dr. Starr added Trental to that. The patient states that over the years, she continued to have the numbness and tingling episodes of the right side of her face. The last several seconds at times, rarely
Here they concentrate more on the iron and aluminum mass in the hippocampus. According to this studied the Alzheimer’s disease has similar symptoms to dementia pugilstica .Patients with punch drunk (dementia pugilistica) showed sign such as aggressive behavior. The similarities between the syndromes between Alzheimer’s disease and Punch drunk, and also between the deficits may suggest that this two diseases have similar etiological mechanism which means the reasons caused these two are the same. The symptoms such as having an aggressive behavior is explained by having smaller amount of Purkinje cells, also ventricles are becoming bigger than normal size. The reason for those symptoms are repetitive brain injuries in case of boxing getting repetitive hits on the heads of boxers. Bur the most important problem in punch drunk syndrome is that neurofibrillary tangles (NFT) are being developed. The statement about NFT again brings to the ide about similarities between Alzheimer’s disease and punch drunk syndrome but there is difference between distributions of it in both cases. In AD (Alzheimer’s disease) it has been seen in deeper levels. But however NFT had higher level of Al and Fe in punch drunk syndrome than in Alzheimer’s
The effects associated with alcohol are produced by the ethanol in the alcohol. The severity of these effects is reflected by the concentration of alcohol in an individual’s blood, which is dictated by the amount of alcohol ingested, the volume of blood, the individual’s metabolism, and amount of time since ingestion. In large doses, alcohol acts as a depressant of the central nervous-system. A blood alcohol level of 0.1% affects some of the motor areas of the brain associated with speech, balance and manual dexterity. A blood alcohol level of 0.2% depresses all motor functions and the area concerned with emotions is depressed. At a blood alcohol level of 0.45% the entire section of the brain that handles perception is depressed and the individual becomes comatose. At a blood alcohol level of 0.7% the parts of the brain that control the heartbeat and breathing are depressed and the individual
In Jill Dombrauckas’s (2015) report, she discussed that the Pennsylvania DUI Association made a large amount of researches about alcohol’s effect on body systems. In one research, alcohol affects the central nervous system which means when the individual drink alcohol, the messages that are carried to and from the brain and the body’s muscles can be slowed delivery. For example, the incoming signals from the brain, like the painful sensory that will decrease the injury’s awareness. Also the signals from the brain to the muscles will lead the motor skills becoming insensitive.
Chronic alcoholic myopathy diagnosis is linked with a number of problems; it is not accompanied by an increase in the blood plasma CPK level, the performance of electromyography does not show changes in the form of decreased MUAP amplitude and duration and increased number of polyphasic MUAP typical of the primary muscular level of damage.12