1. Nonketotic hyperglycemia (NKH) is a clinical syndrome characterized by severe hyperglycemia, hyperosmolarity, and intracellular dehydration without ketoacidosis. It commonly presents with neurological symptoms like seizures, visual hallucinations, and hemichorea.
2. Seizures are reported in up to 25% of NKH cases and can be the first sign of diabetes. The most common type of seizure seen is epilepsia partialis continua, which involves occipital or aphasic seizures.
3. The pathogenesis of seizures in NKH is still unclear but may involve osmotic changes from hyperglycemia, low gamma-aminobutyric acid
A 17-year-old female presented with seizures for the past 6 months. On examination, she was found to have hypocalcemia with a serum calcium level of 5.7 mg/dl. Further workup revealed low levels of parathyroid hormone, indicating hypoparathyroidism as the cause of her hypocalcemia and seizures. Brain CT and EEG were normal. She was started on calcium and vitamin D supplementation, which improved her symptoms and lab abnormalities.
This document describes a case of Miller Fisher syndrome in a 24-year-old female patient presenting with gait instability, facial weakness, eye movement abnormalities, limb numbness, and dysphagia. Electrodiagnostic testing showed normal nerve conduction but abnormal sensory Ia afferent conduction, supporting a diagnosis of Miller Fisher syndrome. Key findings included hypotonia, areflexia, loss of the H-reflex, and decreased sensory evoked potentials attributed to increased intracranial pressure. The multiple cranial neuropathies with normal MRI and abnormal afferent conduction established a diagnosis of Miller Fisher syndrome associated with benign intracranial hypertension.
A 57-year-old diabetic man presented with double vision for 6 days and difficulty walking for 4 days. On examination, he had bilateral eye muscle paralysis, weakness of the limbs, reduced reflexes, and an unsteady gait. Tests showed a motor nerve disorder and diabetes complications. He was diagnosed with Guillain-Barré syndrome (Miller Fisher variant), diabetes mellitus type 2, and white matter brain changes. He received treatment and showed improvement in the hospital.
Dr. sarah weckhuysen kcnq2 Cure summit parent track learn more at kcnq2cure.orgscottyandjim
This document discusses KCNQ2 gene mutations which can cause different epilepsy phenotypes from benign familial neonatal seizures (BFNS) to more severe early-onset epileptic encephalopathy. It describes the discovery of KCNQ2 mutations in BFNS in 1998 and more recent findings of de novo missense mutations in 10% of patients with treatment-resistant neonatal epileptic encephalopathy. These mutations have a dominant-negative effect on channel function and cause neuronal hyperexcitability. The document also reviews other ion channel mutations associated with epilepsy phenotypes along a spectrum, such as SCN1A mutations which can cause GEFS+ or more severe Dravet syndrome.
A 40-year-old legally blind female presented with bilateral lower extremity weakness and inability to walk. She has a history of similar episodes since age 16 diagnosed as a demyelinating disorder. Her current presentation is her worst episode yet with more rapid progression of symptoms and new bowel incontinence. Imaging showed a T6 spinal cord lesion. Laboratory tests confirmed high aquaporin-4 antibody levels consistent with Neuromyelitis Optica Spectrum Disorder. The neurologist recommended additional treatments like Rituximab or plasma exchange but the patient wished to try steroids first.
This document discusses diabetic neuropathy. It defines diabetic neuropathy as nerve dysfunction in people with diabetes after excluding other causes. Diabetic neuropathy can involve both sensory and autonomic nerves and manifest as distal symmetrical polyneuropathy, focal or asymmetrical neuropathies, or combinations. Risk factors include poor glycemic control, hypertension, smoking, and genetics. Diagnosis involves clinical exam and electrodiagnostic testing. Management focuses on glycemic control and treating symptoms.
A 35-year-old diabetic woman presented with altered consciousness for 12 days. She had a history of vomiting and abdominal pain. Examinations revealed she was disoriented with hypertonia and exaggerated reflexes. Investigations showed hyponatremia that had since corrected. MRI brain showed changes consistent with osmotic demyelination syndrome. She was diagnosed with diabetes, osmotic demyelination from hyponatremia, and erosive gastritis. She was treated with insulin, omeprazole, rehabilitation and discharged with advice to follow up in neurology.
This document presents a case report of organophosphate poisoning in a 2-year-old child who ingested malathion. It outlines the patient's presentation, management, progress, investigations and discharge. It also provides background information on organophosphate poisoning including pathophysiology, effects on different organ systems, grading of severity, management principles and potential complications.
A 17-year-old female presented with seizures for the past 6 months. On examination, she was found to have hypocalcemia with a serum calcium level of 5.7 mg/dl. Further workup revealed low levels of parathyroid hormone, indicating hypoparathyroidism as the cause of her hypocalcemia and seizures. Brain CT and EEG were normal. She was started on calcium and vitamin D supplementation, which improved her symptoms and lab abnormalities.
This document describes a case of Miller Fisher syndrome in a 24-year-old female patient presenting with gait instability, facial weakness, eye movement abnormalities, limb numbness, and dysphagia. Electrodiagnostic testing showed normal nerve conduction but abnormal sensory Ia afferent conduction, supporting a diagnosis of Miller Fisher syndrome. Key findings included hypotonia, areflexia, loss of the H-reflex, and decreased sensory evoked potentials attributed to increased intracranial pressure. The multiple cranial neuropathies with normal MRI and abnormal afferent conduction established a diagnosis of Miller Fisher syndrome associated with benign intracranial hypertension.
A 57-year-old diabetic man presented with double vision for 6 days and difficulty walking for 4 days. On examination, he had bilateral eye muscle paralysis, weakness of the limbs, reduced reflexes, and an unsteady gait. Tests showed a motor nerve disorder and diabetes complications. He was diagnosed with Guillain-Barré syndrome (Miller Fisher variant), diabetes mellitus type 2, and white matter brain changes. He received treatment and showed improvement in the hospital.
Dr. sarah weckhuysen kcnq2 Cure summit parent track learn more at kcnq2cure.orgscottyandjim
This document discusses KCNQ2 gene mutations which can cause different epilepsy phenotypes from benign familial neonatal seizures (BFNS) to more severe early-onset epileptic encephalopathy. It describes the discovery of KCNQ2 mutations in BFNS in 1998 and more recent findings of de novo missense mutations in 10% of patients with treatment-resistant neonatal epileptic encephalopathy. These mutations have a dominant-negative effect on channel function and cause neuronal hyperexcitability. The document also reviews other ion channel mutations associated with epilepsy phenotypes along a spectrum, such as SCN1A mutations which can cause GEFS+ or more severe Dravet syndrome.
A 40-year-old legally blind female presented with bilateral lower extremity weakness and inability to walk. She has a history of similar episodes since age 16 diagnosed as a demyelinating disorder. Her current presentation is her worst episode yet with more rapid progression of symptoms and new bowel incontinence. Imaging showed a T6 spinal cord lesion. Laboratory tests confirmed high aquaporin-4 antibody levels consistent with Neuromyelitis Optica Spectrum Disorder. The neurologist recommended additional treatments like Rituximab or plasma exchange but the patient wished to try steroids first.
This document discusses diabetic neuropathy. It defines diabetic neuropathy as nerve dysfunction in people with diabetes after excluding other causes. Diabetic neuropathy can involve both sensory and autonomic nerves and manifest as distal symmetrical polyneuropathy, focal or asymmetrical neuropathies, or combinations. Risk factors include poor glycemic control, hypertension, smoking, and genetics. Diagnosis involves clinical exam and electrodiagnostic testing. Management focuses on glycemic control and treating symptoms.
A 35-year-old diabetic woman presented with altered consciousness for 12 days. She had a history of vomiting and abdominal pain. Examinations revealed she was disoriented with hypertonia and exaggerated reflexes. Investigations showed hyponatremia that had since corrected. MRI brain showed changes consistent with osmotic demyelination syndrome. She was diagnosed with diabetes, osmotic demyelination from hyponatremia, and erosive gastritis. She was treated with insulin, omeprazole, rehabilitation and discharged with advice to follow up in neurology.
This document presents a case report of organophosphate poisoning in a 2-year-old child who ingested malathion. It outlines the patient's presentation, management, progress, investigations and discharge. It also provides background information on organophosphate poisoning including pathophysiology, effects on different organ systems, grading of severity, management principles and potential complications.
A 17-year-old man presented with ascending weakness over 2 weeks, difficulty swallowing, and a changed voice for 1 week. On examination, he had decreased tone and weakness in both upper and lower limbs along with absent reflexes. Nerve conduction studies revealed findings consistent with demyelinating polyneuropathy. He was diagnosed with acute inflammatory demyelinating polyneuropathy (AIDP).
This document summarizes a case study of a 14-year-old girl presenting with progressive muscle weakness over 10 days. Her examination showed diminished and symmetric muscle strength, loss of vibratory sense, absent reflexes, and impaired handling of secretions. Investigations including lumbar puncture, MRI, and bloodwork were normal. The diagnosis was Guillain-Barré syndrome based on the clinical presentation and findings.
José L. Ruiz-Sandoval, Erwin Chiquete,
Lucía E. Álvarez-Palazuelos, Miguel
A. Andrade-Ramos & Luis R. Rodríguez-
Rubio
Osmotic demyelination syndrome (ODS) is the
damage over the central nervous system caused by several
electrolytes, metabolic and toxic disorders. We aimed to
describe cases of unusual forms of ODS. In a 9-year period,
25 consecutive patients with ODS (15 men; mean age
42 years) were registered in our referral institution, among
them, four (16 %) with atypical neuroimaging findings
were abstracted for this communication. None of them
presented cardiorespiratory arrest, head trauma, seizures,
neuromyelitis optica spectrum or contact with toxic
chemicals. Case 1 was a 33-year-old alcoholic man without
hypertension or electrolyte imbalance, who presented a
classic central pontine myelinolysis (CPM) and a hemorrhage
within the pons. Case 2 was a 34-year-old alcoholic
man with hypoglycemia and hyponatremia who presented
CPM and diffuse bihemispheric extrapontine myelinolysis
(EPM) after correction of serum sodium. Case 3 was a
52-year-old woman with mild hypokalemia and hyponatremia
(inadequately corrected), who presented a peduncular
and cerebellar EPM. Case 4 was a 67-year-old
woman who had a suicidal attempt with antidepressants
and carbamazepine without impaired consciousness, who
complicated with mild hyponatremia associated with a
classical CPM and a spinal cord EPM. Case 2 died and the
rest remained with variable neurological impairments at
last follow-up visit. With modern neuroimaging, the
so-called atypical forms of ODS may not be as rare as
previously thought; however, they could have a more
adverse outcome than the classical ODS.
Dr. sarah weckhuysen kcnq2 Cure summit professional track - Lean more at kcn...scottyandjim
This document summarizes current research on KCNQ2 mutations and KCNQ2 encephalopathy. It discusses how KCNQ2 mutations were discovered in patients with benign familial neonatal seizures (BFNS) in 1998. More recently, de novo KCNQ2 mutations have been found to cause KCNQ2 encephalopathy, an early-onset epileptic encephalopathy associated with intellectual disability. These mutations have a dominant negative effect on channel function. Retigabine, a potassium channel opener, shows promise in treating seizures caused by KCNQ2 encephalopathy. Further research is needed to better understand genotype-phenotype correlations, treatment responses, functional consequences of mutations, and potential therapies.
Epilepsy case presentation by mehreen taj IVth parm DMehreen taj
Epilepsy:Epilepsy occurs when permanent changes in brain tissue cause the brain to be too excitable or jumpy. The brain sends out abnormal signals. This results in repeated, unpredictable seizures. (A single seizure that does not happen again is not epilepsy.Epilepsy is a disorder with many possible causes. Anything that disturbs the normal pattern of neuron activity -- from illness to brain damage to abnormal brain development -- can lead to seizures.The main causes of Epilepsy and resultant seizures include Meningitis, head injury or trauma, stroke, brain tumour, high fever (Febrile Seizure), and parasite infection Neuro-cysticercosis. The main triggering factors include light, noise, sleep loss, alcohol intake and cigarette smoking.
Epileptic seizures vary in intensity and symptoms depending on what part of the brain is involved. In partial seizures, the most common form of seizure in adults, only one area of the brain is involved. Partial seizures are classified as simple partial, complex partial (also known as psychomotor), and absence (also known as myoclonic or petit mal) seizure.
• Definition
• Causes
• Pathophysiology
• Assessment and common findings p 882,/p 899 PCCM 216
o Petit mal
o Grand mal
o Partial seizures
o Complex partial seizure
• Management p 882/p 899 / PCCM 216
o Drug therapy
o Break through seizure PCC M 218
• Complications
• Status epilepticus p 883/p 900 / PCCM 219 (T&E Periods)
o Definition
o Effects
o Causes
o Management
• Essential health information p 883/p 900 PCCM 217
o General
o Seizure diary
o Drug interaction vigilance
o Lifestyle education
• Convulsions in children p 883/p 900
• Epilepsy in the elderly p 1058/ p1087
Dr. john millichap kcnq2 Cure summit professional track learn more at kcnq2cu...scottyandjim
Dr. John Millichap speaking at 2014 Denver KCNQ2 Cure summit professionals track at Children's Hospital of Colorado. More information at www.kcnq2cure.org
1) A 58-year old male developed central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) four days after being discharged from the ICU following treatment for hyponatremia.
2) CPM was first described in 1959 as a demyelinating condition affecting the pons seen in alcoholic and malnourished patients. Subsequent studies found it can result from rapid correction of hyponatremia.
3) The pathogenesis of CPM/EPM involves rapid correction of hyponatremia causing an osmotic gradient that opens the blood-brain barrier, allowing blood factors to enter and cause demyelination. The specific
Medical conditions with NeuroPsychiatric problemsVindisel Marconi
The document discusses various medical conditions that can cause neuropsychiatric symptoms. It covers conditions in several categories - infectious diseases like COVID-19, HIV, syphilis and Lyme disease; rheumatologic/autoimmune diseases like systemic lupus erythematosus and sarcoidosis; endocrinologic diseases like thyroid disorders and Cushing syndrome; metabolic conditions involving vitamin deficiencies, calcium levels, porphyrias and Wilson's disease; neoplastic causes from paraneoplastic syndromes; and neurological disorders like multiple sclerosis. For each condition, it describes the pathophysiology and potential neuropsychiatric manifestations.
Status epilepticus is a medical emergency defined as a seizure lasting more than 5 minutes or recurrent seizures without regaining consciousness. It can be convulsive, involving motor symptoms, or non-convulsive without obvious symptoms but still involving abnormal brain activity. Causes include prior epilepsy, trauma, infection, drugs or metabolic imbalances. Treatment aims to stop seizures quickly with benzodiazepines or anti-seizure drugs to prevent complications like cardiac or respiratory issues, metabolic disturbances and neuronal damage. Prolonged status epilepticus can lead to a refractory state requiring intensive care management to prevent disability or death.
A 25-year-old man presented with seizures and was found to have neurocysticercosis based on imaging findings. MRI showed multiple hypo-intense brain lesions on T1W and FLAIR sequences that were hyper-intense on T2WI, with a central nodule in each lesion. He was treated with albendazole and a VP shunt was placed for associated hydrocephalus. Follow-up imaging showed decreased lesion size and resolution of hydrocephalus. Neurocysticercosis results from Taenia solium infection and can cause seizures, hydrocephalus, and other neurological symptoms.
1) Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a rare acquired neuropathy accounting for 1-2 cases per 100,000 people, most commonly affecting males in the 5th-6th decades of life.
2) It is characterized by progressive weakness and sensory loss in both the proximal and distal portions of the limbs and can involve the cranial nerves. Diagnosis requires supportive electrophysiology and cerebrospinal fluid analysis.
3) Treatment involves immunotherapies like intravenous immunoglobulin, plasma exchange, or corticosteroids to reduce inflammation and prevent disability. Most patients respond well but some may require additional immunosuppressive agents and long-
Refractory Status epilepticus: A Time TravelWafik Bahnasy
Status Epilepticus is a condition resulting from failure of the mechanisms responsible for seizure termination or the initiation of mechanisms, which leads to abnormally prolonged seizures (time point, T1) that might have long-term consequences (time point T2), including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures.
Diagnosis and management of status epilepticusSheela Aglecha
Status epilepticus is defined as continuous seizure activity or recurrent seizures without regaining consciousness lasting more than 5 minutes. It is most common in children under 5 years old, with an incidence over 100 per 100,000 children in this age group. The document outlines various etiologies and risk factors for status epilepticus as well as treatments including anesthetic doses of midazolam, phenobarbital, ketamine or propofol administered via bolus or infusion. There is no clear evidence to guide therapy after initial treatment failure, but additional options discussed include inhaled anesthetics, the ketogenic diet, epilepsy surgery, hypothermia, immunotherapy, and electroconvulsive therapy.
A 33-year-old male presented with sudden onset weakness of the limbs for 7 hours. He has a history of similar episodes in the summer after excessive work. On examination, he had weakness of proximal and distal muscles of all limbs. Laboratory tests found hypokalemia, metabolic alkalosis, hypomagnesium, and low urinary calcium levels. He was diagnosed with Gitelman's syndrome based on the clinical and laboratory findings. Gitelman's syndrome is an autosomal recessive disorder characterized by hypokalemia, metabolic alkalosis, hypomagnesium, hypocalciuria, and normal blood pressure.
A 48-year-old female presented with double vision, inability to close her left eye, redness of the left eye, difficulty swallowing, and unsteadiness while walking over the past 3 days. On examination, she had right lateral rectus palsy, left facial weakness, gait ataxia, and proximal weakness of the lower limbs. Investigations showed multi-nodular goiter and demyelinating radiculopathy more severe in the lower limbs. She was diagnosed with Miller Fisher syndrome/Bickerstaff brainstem encephalitis overlap and treated with plasma exchange, with improvement of symptoms over time.
Progressive myoclonic epilepsy (PME) is a group of rare neurodegenerative diseases characterized by myoclonus, progressive neurological decline, and epileptic seizures. There are several known genetic causes of PME, which can make diagnosis challenging. Treatment focuses on controlling seizures and symptoms, though most forms of PME are ultimately severe and disabling. Genetic testing may help identify the specific form to improve diagnosis and guidance around prognosis.
HISTORY : Description about seizure activity.
Age of Onset.
Duration.
Focal / Generalized.
Loss of conciousness, associated features .
H/o previous attack.
H/O Trauma, Drug ingestion.
Hypokalemic Periodic Paralysis A Case Reportijtsrd
"Hypokalemic periodic paralysis HPP is a medical emergency with prevalence of 1 in 100,000 . Rapid management is very important since, very low potassium levels can lead to cardiac complications . In this case, a twenty four year old female without a similar history in the family, having hypokalemia periodic paralysis attack is presented. This case report study has been presented for the consideration of the rare HPP in patients presenting with sudden muscle weakness. Blessy Rachal Boban | Cillamol K. J | Elena Cheruvil | Sheffin Thomas | Tony Abraham ""Hypokalemic Periodic Paralysis: A Case Report"" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-3 | Issue-3 , April 2019, URL: https://www.ijtsrd.com/papers/ijtsrd21658.pdf
Paper URL: https://www.ijtsrd.com/pharmacy/pharmacy-practice/21658/hypokalemic-periodic-paralysis-a-case-report/blessy-rachal-boban"
1) Diabetic neuropathy is a syndrome comprising separate clinical disorders that affect the peripheral nervous system, with a prevalence of 66% for type 1 diabetes and 59% for type 2 diabetes.
2) Risk factors include hyperglycemia, longer duration of diabetes, age, hypertension, and smoking.
3) The most common form is distal symmetrical sensorimotor polyneuropathy, which involves small and large fiber sensory, autonomic, and motor nerves in various combinations.
Movement disorders: A complication of chronic hyperglycemia? A case reportApollo Hospitals
A 77-year-old man presented with bilateral choreic movements that had developed over the past month. He had a history of poorly controlled type 2 diabetes. At admission, he was found to have severe hyperglycemia without ketosis. A CT scan showed hyperdensity in the putamen and lenticular nucleus. Treatment with insulin, haloperidol, and glycemic control led to regression of the choreic movements within 4 days. Chorea secondary to nonketotic hyperglycemia is a rare complication of uncontrolled diabetes that is usually reversible with normalization of blood glucose levels and neuroleptic treatment. The pathophysiology is thought to involve metabolic disturbances from hyperglycemia impairing neurotransmission in basal ganglia structures and
Movement disorders: A complication of chronic Hyperglycemia? A case reportApollo Hospitals
This case report describes a 77-year-old man who presented with bilateral choreic movements that were predominantly on the right side, along with some dystonic movements. He had long-standing type 2 diabetes that was poorly controlled, with an HbA1c of 17.3%. Brain imaging showed hyperdensity in the putamen and lenticular nucleus. His symptoms improved with insulin treatment and a neuroleptic medication. The report discusses that uncontrolled diabetes can rarely cause movement disorders like chorea due to metabolic disturbances in the basal ganglia from hyperglycemia. Prompt treatment of the hyperglycemia typically leads to resolution of the neurological symptoms.
A 17-year-old man presented with ascending weakness over 2 weeks, difficulty swallowing, and a changed voice for 1 week. On examination, he had decreased tone and weakness in both upper and lower limbs along with absent reflexes. Nerve conduction studies revealed findings consistent with demyelinating polyneuropathy. He was diagnosed with acute inflammatory demyelinating polyneuropathy (AIDP).
This document summarizes a case study of a 14-year-old girl presenting with progressive muscle weakness over 10 days. Her examination showed diminished and symmetric muscle strength, loss of vibratory sense, absent reflexes, and impaired handling of secretions. Investigations including lumbar puncture, MRI, and bloodwork were normal. The diagnosis was Guillain-Barré syndrome based on the clinical presentation and findings.
José L. Ruiz-Sandoval, Erwin Chiquete,
Lucía E. Álvarez-Palazuelos, Miguel
A. Andrade-Ramos & Luis R. Rodríguez-
Rubio
Osmotic demyelination syndrome (ODS) is the
damage over the central nervous system caused by several
electrolytes, metabolic and toxic disorders. We aimed to
describe cases of unusual forms of ODS. In a 9-year period,
25 consecutive patients with ODS (15 men; mean age
42 years) were registered in our referral institution, among
them, four (16 %) with atypical neuroimaging findings
were abstracted for this communication. None of them
presented cardiorespiratory arrest, head trauma, seizures,
neuromyelitis optica spectrum or contact with toxic
chemicals. Case 1 was a 33-year-old alcoholic man without
hypertension or electrolyte imbalance, who presented a
classic central pontine myelinolysis (CPM) and a hemorrhage
within the pons. Case 2 was a 34-year-old alcoholic
man with hypoglycemia and hyponatremia who presented
CPM and diffuse bihemispheric extrapontine myelinolysis
(EPM) after correction of serum sodium. Case 3 was a
52-year-old woman with mild hypokalemia and hyponatremia
(inadequately corrected), who presented a peduncular
and cerebellar EPM. Case 4 was a 67-year-old
woman who had a suicidal attempt with antidepressants
and carbamazepine without impaired consciousness, who
complicated with mild hyponatremia associated with a
classical CPM and a spinal cord EPM. Case 2 died and the
rest remained with variable neurological impairments at
last follow-up visit. With modern neuroimaging, the
so-called atypical forms of ODS may not be as rare as
previously thought; however, they could have a more
adverse outcome than the classical ODS.
Dr. sarah weckhuysen kcnq2 Cure summit professional track - Lean more at kcn...scottyandjim
This document summarizes current research on KCNQ2 mutations and KCNQ2 encephalopathy. It discusses how KCNQ2 mutations were discovered in patients with benign familial neonatal seizures (BFNS) in 1998. More recently, de novo KCNQ2 mutations have been found to cause KCNQ2 encephalopathy, an early-onset epileptic encephalopathy associated with intellectual disability. These mutations have a dominant negative effect on channel function. Retigabine, a potassium channel opener, shows promise in treating seizures caused by KCNQ2 encephalopathy. Further research is needed to better understand genotype-phenotype correlations, treatment responses, functional consequences of mutations, and potential therapies.
Epilepsy case presentation by mehreen taj IVth parm DMehreen taj
Epilepsy:Epilepsy occurs when permanent changes in brain tissue cause the brain to be too excitable or jumpy. The brain sends out abnormal signals. This results in repeated, unpredictable seizures. (A single seizure that does not happen again is not epilepsy.Epilepsy is a disorder with many possible causes. Anything that disturbs the normal pattern of neuron activity -- from illness to brain damage to abnormal brain development -- can lead to seizures.The main causes of Epilepsy and resultant seizures include Meningitis, head injury or trauma, stroke, brain tumour, high fever (Febrile Seizure), and parasite infection Neuro-cysticercosis. The main triggering factors include light, noise, sleep loss, alcohol intake and cigarette smoking.
Epileptic seizures vary in intensity and symptoms depending on what part of the brain is involved. In partial seizures, the most common form of seizure in adults, only one area of the brain is involved. Partial seizures are classified as simple partial, complex partial (also known as psychomotor), and absence (also known as myoclonic or petit mal) seizure.
• Definition
• Causes
• Pathophysiology
• Assessment and common findings p 882,/p 899 PCCM 216
o Petit mal
o Grand mal
o Partial seizures
o Complex partial seizure
• Management p 882/p 899 / PCCM 216
o Drug therapy
o Break through seizure PCC M 218
• Complications
• Status epilepticus p 883/p 900 / PCCM 219 (T&E Periods)
o Definition
o Effects
o Causes
o Management
• Essential health information p 883/p 900 PCCM 217
o General
o Seizure diary
o Drug interaction vigilance
o Lifestyle education
• Convulsions in children p 883/p 900
• Epilepsy in the elderly p 1058/ p1087
Dr. john millichap kcnq2 Cure summit professional track learn more at kcnq2cu...scottyandjim
Dr. John Millichap speaking at 2014 Denver KCNQ2 Cure summit professionals track at Children's Hospital of Colorado. More information at www.kcnq2cure.org
1) A 58-year old male developed central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) four days after being discharged from the ICU following treatment for hyponatremia.
2) CPM was first described in 1959 as a demyelinating condition affecting the pons seen in alcoholic and malnourished patients. Subsequent studies found it can result from rapid correction of hyponatremia.
3) The pathogenesis of CPM/EPM involves rapid correction of hyponatremia causing an osmotic gradient that opens the blood-brain barrier, allowing blood factors to enter and cause demyelination. The specific
Medical conditions with NeuroPsychiatric problemsVindisel Marconi
The document discusses various medical conditions that can cause neuropsychiatric symptoms. It covers conditions in several categories - infectious diseases like COVID-19, HIV, syphilis and Lyme disease; rheumatologic/autoimmune diseases like systemic lupus erythematosus and sarcoidosis; endocrinologic diseases like thyroid disorders and Cushing syndrome; metabolic conditions involving vitamin deficiencies, calcium levels, porphyrias and Wilson's disease; neoplastic causes from paraneoplastic syndromes; and neurological disorders like multiple sclerosis. For each condition, it describes the pathophysiology and potential neuropsychiatric manifestations.
Status epilepticus is a medical emergency defined as a seizure lasting more than 5 minutes or recurrent seizures without regaining consciousness. It can be convulsive, involving motor symptoms, or non-convulsive without obvious symptoms but still involving abnormal brain activity. Causes include prior epilepsy, trauma, infection, drugs or metabolic imbalances. Treatment aims to stop seizures quickly with benzodiazepines or anti-seizure drugs to prevent complications like cardiac or respiratory issues, metabolic disturbances and neuronal damage. Prolonged status epilepticus can lead to a refractory state requiring intensive care management to prevent disability or death.
A 25-year-old man presented with seizures and was found to have neurocysticercosis based on imaging findings. MRI showed multiple hypo-intense brain lesions on T1W and FLAIR sequences that were hyper-intense on T2WI, with a central nodule in each lesion. He was treated with albendazole and a VP shunt was placed for associated hydrocephalus. Follow-up imaging showed decreased lesion size and resolution of hydrocephalus. Neurocysticercosis results from Taenia solium infection and can cause seizures, hydrocephalus, and other neurological symptoms.
1) Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a rare acquired neuropathy accounting for 1-2 cases per 100,000 people, most commonly affecting males in the 5th-6th decades of life.
2) It is characterized by progressive weakness and sensory loss in both the proximal and distal portions of the limbs and can involve the cranial nerves. Diagnosis requires supportive electrophysiology and cerebrospinal fluid analysis.
3) Treatment involves immunotherapies like intravenous immunoglobulin, plasma exchange, or corticosteroids to reduce inflammation and prevent disability. Most patients respond well but some may require additional immunosuppressive agents and long-
Refractory Status epilepticus: A Time TravelWafik Bahnasy
Status Epilepticus is a condition resulting from failure of the mechanisms responsible for seizure termination or the initiation of mechanisms, which leads to abnormally prolonged seizures (time point, T1) that might have long-term consequences (time point T2), including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures.
Diagnosis and management of status epilepticusSheela Aglecha
Status epilepticus is defined as continuous seizure activity or recurrent seizures without regaining consciousness lasting more than 5 minutes. It is most common in children under 5 years old, with an incidence over 100 per 100,000 children in this age group. The document outlines various etiologies and risk factors for status epilepticus as well as treatments including anesthetic doses of midazolam, phenobarbital, ketamine or propofol administered via bolus or infusion. There is no clear evidence to guide therapy after initial treatment failure, but additional options discussed include inhaled anesthetics, the ketogenic diet, epilepsy surgery, hypothermia, immunotherapy, and electroconvulsive therapy.
A 33-year-old male presented with sudden onset weakness of the limbs for 7 hours. He has a history of similar episodes in the summer after excessive work. On examination, he had weakness of proximal and distal muscles of all limbs. Laboratory tests found hypokalemia, metabolic alkalosis, hypomagnesium, and low urinary calcium levels. He was diagnosed with Gitelman's syndrome based on the clinical and laboratory findings. Gitelman's syndrome is an autosomal recessive disorder characterized by hypokalemia, metabolic alkalosis, hypomagnesium, hypocalciuria, and normal blood pressure.
A 48-year-old female presented with double vision, inability to close her left eye, redness of the left eye, difficulty swallowing, and unsteadiness while walking over the past 3 days. On examination, she had right lateral rectus palsy, left facial weakness, gait ataxia, and proximal weakness of the lower limbs. Investigations showed multi-nodular goiter and demyelinating radiculopathy more severe in the lower limbs. She was diagnosed with Miller Fisher syndrome/Bickerstaff brainstem encephalitis overlap and treated with plasma exchange, with improvement of symptoms over time.
Progressive myoclonic epilepsy (PME) is a group of rare neurodegenerative diseases characterized by myoclonus, progressive neurological decline, and epileptic seizures. There are several known genetic causes of PME, which can make diagnosis challenging. Treatment focuses on controlling seizures and symptoms, though most forms of PME are ultimately severe and disabling. Genetic testing may help identify the specific form to improve diagnosis and guidance around prognosis.
HISTORY : Description about seizure activity.
Age of Onset.
Duration.
Focal / Generalized.
Loss of conciousness, associated features .
H/o previous attack.
H/O Trauma, Drug ingestion.
Hypokalemic Periodic Paralysis A Case Reportijtsrd
"Hypokalemic periodic paralysis HPP is a medical emergency with prevalence of 1 in 100,000 . Rapid management is very important since, very low potassium levels can lead to cardiac complications . In this case, a twenty four year old female without a similar history in the family, having hypokalemia periodic paralysis attack is presented. This case report study has been presented for the consideration of the rare HPP in patients presenting with sudden muscle weakness. Blessy Rachal Boban | Cillamol K. J | Elena Cheruvil | Sheffin Thomas | Tony Abraham ""Hypokalemic Periodic Paralysis: A Case Report"" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-3 | Issue-3 , April 2019, URL: https://www.ijtsrd.com/papers/ijtsrd21658.pdf
Paper URL: https://www.ijtsrd.com/pharmacy/pharmacy-practice/21658/hypokalemic-periodic-paralysis-a-case-report/blessy-rachal-boban"
1) Diabetic neuropathy is a syndrome comprising separate clinical disorders that affect the peripheral nervous system, with a prevalence of 66% for type 1 diabetes and 59% for type 2 diabetes.
2) Risk factors include hyperglycemia, longer duration of diabetes, age, hypertension, and smoking.
3) The most common form is distal symmetrical sensorimotor polyneuropathy, which involves small and large fiber sensory, autonomic, and motor nerves in various combinations.
Movement disorders: A complication of chronic hyperglycemia? A case reportApollo Hospitals
A 77-year-old man presented with bilateral choreic movements that had developed over the past month. He had a history of poorly controlled type 2 diabetes. At admission, he was found to have severe hyperglycemia without ketosis. A CT scan showed hyperdensity in the putamen and lenticular nucleus. Treatment with insulin, haloperidol, and glycemic control led to regression of the choreic movements within 4 days. Chorea secondary to nonketotic hyperglycemia is a rare complication of uncontrolled diabetes that is usually reversible with normalization of blood glucose levels and neuroleptic treatment. The pathophysiology is thought to involve metabolic disturbances from hyperglycemia impairing neurotransmission in basal ganglia structures and
Movement disorders: A complication of chronic Hyperglycemia? A case reportApollo Hospitals
This case report describes a 77-year-old man who presented with bilateral choreic movements that were predominantly on the right side, along with some dystonic movements. He had long-standing type 2 diabetes that was poorly controlled, with an HbA1c of 17.3%. Brain imaging showed hyperdensity in the putamen and lenticular nucleus. His symptoms improved with insulin treatment and a neuroleptic medication. The report discusses that uncontrolled diabetes can rarely cause movement disorders like chorea due to metabolic disturbances in the basal ganglia from hyperglycemia. Prompt treatment of the hyperglycemia typically leads to resolution of the neurological symptoms.
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinar...Jack Frost
The document presents a case study on a 37-year-old male patient, G.M., who was admitted to the hospital with complaints of lower extremity weakness. He was diagnosed with severe hypokalemia, hypoxic ischemic encephalopathy, nosocomial pneumonia, and a urinary tract infection. The patient experienced respiratory arrest and was intubated. He was treated with potassium supplements to address his hypokalemia and given antibiotics to treat his pneumonia and urinary tract infection. His conditions developed as complications during his hospital stay.
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinar...Jack Frost
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinary Tract Infection. This presentation contains real names of persons involve of this particular study. This names should not be copied or rewritten. Used the data of this study as basis only. All rights reserved 2009.
Porphyrias and neurological menifestationsNeurologyKota
This document summarizes the rare metabolic disorders known as porphyrias, which result from defects in the heme biosynthesis pathway. Heme is essential for oxygen transport and energy production. The document describes the different types of porphyrias, which can be hepatic or erythropoietic in origin and inherited in autosomal dominant, recessive, or X-linked patterns. The major types that cause neurological symptoms are acute intermittent porphyria, hereditary coproporphyria, and variegate porphyria. Neurological manifestations include autonomic neuropathy, peripheral neuropathy, and encephalopathy. Treatment involves administering heme or carbohydrate precursors to reduce accumulation of toxic heme intermediates.
Metabolic disoders internal medicine and neuroscienceNeilVincentDeAsis
This document discusses acquired metabolic disorders of the nervous system that result from failure of other organ systems. It focuses on hypoxic-ischemic encephalopathy, where lack of oxygen and blood flow to the brain causes global disturbance of cerebral function. The main causes are discussed as well as the clinical features and progression from confusion to stupor and coma. Laboratory tests that can help identify potential causes are also outlined.
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
status epilepticus in child je workshop mksdrmksped
Status epilepticus is a medical emergency defined as continuous seizure activity lasting more than 30 minutes or recurrent seizures without regaining consciousness between seizures. It requires prompt treatment to prevent neurological injury and death. The document discusses the epidemiology, pathophysiology, treatment, and prognosis of status epilepticus. Initial treatment involves maintaining airway, breathing, and circulation while administering benzodiazepines like lorazepam or diazepam. For refractory cases, additional anticonvulsants like fosphenytoin, phenobarbital, midazolam, or propofol may be used. Outcomes depend on factors like duration and etiology of seizures, with mortality ranging from 3-30
This document provides an overview of osmotic demyelination syndrome (ODS), also known as central pontine myelinolysis. It discusses the history, controversies in nomenclature, pathology, epidemiology, pathophysiology, clinical features, diagnosis, management including prevention, re-lowering sodium levels, supportive care and investigational therapies, prognosis, and key references. The document is intended as an educational resource for physicians on ODS.
This document discusses renal and hepatic encephalopathy. It defines uremic encephalopathy as a brain disorder that occurs in patients with untreated or inadequately treated kidney disease. Symptoms range from mild to severe and fluctuate depending on kidney function. Uremic toxins that accumulate due to renal dysfunction are a primary cause. Treatment involves optimizing dialysis to adequately remove toxins. Other types of encephalopathy discussed include dialysis dementia, central pontine myelinolysis, seizures, and restless leg syndrome. Causes, clinical features, diagnosis and management are described for each condition.
This document discusses possible complications from epilepsy and managing the disease process. It outlines potential complications that can affect cardiac, autonomic, pulmonary, metabolic, endocrine and other body systems. Repeated seizures can also cause issues like rhabdomyolysis and kidney failure. Epilepsy impacts various aspects of life including education, employment, social interactions and relationships. Managing the disease requires taking medications regularly, maintaining a healthy lifestyle, being aware of seizure triggers, and addressing any mental health issues. Two classes of anticonvulsant medications are used to treat epilepsy - very rapidly acting ones for status epilepticus and less rapid acting ones to prevent future seizures.
Hepatic encephalopathy is a reversible neuropsychiatric impairment that ranges from subtle mental status changes to deep coma in patients with acute or chronic liver disease. There are several proposed mechanisms for hepatic encephalopathy, including the ammonia, inflammation, oxidative stress, and manganese theories. The pathogenesis involves toxic substances bypassing the liver and affecting astrocyte function in the brain, which can lead to cerebral edema. Clinical examination is needed to diagnose hepatic encephalopathy and exclude other potential causes of altered mental status in cirrhotic patients.
This document discusses various types of diabetic comas including diabetic ketoacidosis (DKA), hypoglycemic coma, and hyperosmolar non-ketotic coma. It provides details on the etiology, pathogenesis, clinical presentation, and treatment principles for each type of coma. The document also describes classifications of acute and chronic diabetic complications and covers specific complications like nephropathy, retinopathy, neuropathy, and diabetic foot syndrome. Treatment protocols for diabetic ketoacidosis are outlined, focusing on insulin therapy, rehydration, electrolyte correction, and acid-base balance correction.
This document discusses seizures and epilepsy in children. It defines a seizure as abnormal excessive neuronal activity in the brain and epilepsy as two or more unprovoked seizures occurring more than 24 hours apart. Seizures can be focal, originating in one area of the brain, or generalized, involving both hemispheres simultaneously. Epilepsy syndromes are described. Imaging and EEG play roles in evaluating seizures, with MRI being preferred and EEG showing localized or generalized abnormalities.
This document discusses complications that can arise from epilepsy. It notes that epilepsy can affect various body systems like the cardiac, pulmonary, and metabolic systems, potentially leading to complications such as arrhythmias, respiratory issues, and changes in electrolyte levels. The document also outlines how epilepsy can significantly impact one's education, employment, social life, and relationships by causing issues like cognitive impairments, communication problems, and stigma. Managing the condition requires strict medication adherence, a healthy lifestyle, safety precautions, and addressing any mental health issues that may arise from living with epilepsy.
Perinatal asphyxia refers to progressive hypoxia, hypercarbia and acidosis during birth. It can cause multi-organ dysfunction in neonates. The essential criteria for diagnosis are prolonged acidemia on cord blood, low Apgar scores for over 5 minutes, and neurological or multi-organ issues in the newborn period. Asphyxia is caused by factors that limit oxygen delivery to the fetus, such as placental insufficiency, cord accidents, difficult delivery, or postnatal cardiac or respiratory issues. The brain, heart, kidneys and lungs are most commonly affected. Treatment involves resuscitation, controlling seizures, avoiding hyperthermia, and therapeutic hypothermia within 6 hours of birth to reduce neurological
This document discusses convulsive status epilepticus (CSE). It notes that the worldwide incidence of CSE is highest in children and the elderly, with mortality rates ranging from 10.5-28% and neurological sequelae occurring in 11-16% of patients. The most common causes of CSE are listed as low anti-epileptic drug levels, stroke, alcohol withdrawal, anoxic brain injury, and metabolic disturbances. The document provides details on the definition, types, risk factors, complications, management, and treatment of CSE.
EEG in convulsive and non convulsive seizures in the intensive care unitPramod Krishnan
Case based discussion regarding the utility of EEG in the management of convulsive and non convulsive seizures, including status epilepticus in the intensive care unit
Leveraging Generative AI to Drive Nonprofit InnovationTechSoup
In this webinar, participants learned how to utilize Generative AI to streamline operations and elevate member engagement. Amazon Web Service experts provided a customer specific use cases and dived into low/no-code tools that are quick and easy to deploy through Amazon Web Service (AWS.)
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
Philippine Edukasyong Pantahanan at Pangkabuhayan (EPP) CurriculumMJDuyan
(𝐓𝐋𝐄 𝟏𝟎𝟎) (𝐋𝐞𝐬𝐬𝐨𝐧 𝟏)-𝐏𝐫𝐞𝐥𝐢𝐦𝐬
𝐃𝐢𝐬𝐜𝐮𝐬𝐬 𝐭𝐡𝐞 𝐄𝐏𝐏 𝐂𝐮𝐫𝐫𝐢𝐜𝐮𝐥𝐮𝐦 𝐢𝐧 𝐭𝐡𝐞 𝐏𝐡𝐢𝐥𝐢𝐩𝐩𝐢𝐧𝐞𝐬:
- Understand the goals and objectives of the Edukasyong Pantahanan at Pangkabuhayan (EPP) curriculum, recognizing its importance in fostering practical life skills and values among students. Students will also be able to identify the key components and subjects covered, such as agriculture, home economics, industrial arts, and information and communication technology.
𝐄𝐱𝐩𝐥𝐚𝐢𝐧 𝐭𝐡𝐞 𝐍𝐚𝐭𝐮𝐫𝐞 𝐚𝐧𝐝 𝐒𝐜𝐨𝐩𝐞 𝐨𝐟 𝐚𝐧 𝐄𝐧𝐭𝐫𝐞𝐩𝐫𝐞𝐧𝐞𝐮𝐫:
-Define entrepreneurship, distinguishing it from general business activities by emphasizing its focus on innovation, risk-taking, and value creation. Students will describe the characteristics and traits of successful entrepreneurs, including their roles and responsibilities, and discuss the broader economic and social impacts of entrepreneurial activities on both local and global scales.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
"Learn about all the ways Walmart supports nonprofit organizations.
You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
Spark Good (walmart.com/sparkgood) is a charitable platform that enables nonprofits to receive donations directly from customers and associates.
Answers about how you can do more with Walmart!"
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
1. PENDAHULUAN
Hyperglycemia may initially present with neurological manifestations. Diverse
neurological symptoms have been described including: seizures, visual hallucinations,
choreoathetosis, hemiballismus dysphagia, somatosensory symptoms or headache associated
with nausea and vomiting, and severe cases of hyperglycemia can manifest as a coma.1
Epileptic seizure occur in up to 25% of cases of, non-ketotic hyperglycemia (NKH). These
seizures are the first finding of diabetes mellitus in 50% of the patients. The most common
epilepsy is known as epilepsia partialis continua (EPC), Occipital lobe seizures and aphasic
seizures may also be seen in these patients.2
Seizures related to nonketotic hyperglycemia (NKHG) have been reported with
increasing frequency since the first case documented in 1965. The clinical spectrum of this
syndrome is various with a severe course in elderly. It develops more quickly than other
disorders of diabetes mellitus with hyperglycemia, but usually without evidence of ketosis
since the syndrome often ensues during the course of any illness and yet has not been reported
in diverse medical fields, doctors must become familiar with this preventable condition,
especially in elders. Thus, only the prompt institution of appropriate insulin therapy will
improve prognosis and hasten recovery.3
2. LAPORAN KASUS
Seorang pria, 50 tahun, alamat di Kaleosan, pekerjaan petani, dibawa ke IGD tanggal
16 Oktober 2018 dengan riwayat kejang. Kejang dialami pertama kali kurang lebih 3 bulan)
dimana kejang terakhir dialami 3 hari yang lalu. Preiktal : Os sadar dan tidak mengeluh apapun.
Iktal : saat kejang kedua mata mendelik ke kiri, kepala menoleh ke kiri, mulut tidak berbusa,
lidah tergigit dan mengompol. lengan dan tungkai sebelah kiri lurus kaku. Selama kejang
pasien tidak sadar. Kejang dialami selama kurang lebih 1 menit dan berlangsung sebanyak
>20x perhari. Setelah kejang pasien sadar dan cenderung terlihat bingung. Menurut keluarga,
anggota gerak kiri pasien cenderung kurang aktif. 3 bulan terakhir ini Sebelum kejang pasien
tidak mengalami demam, cedera kepala atau nyeri kepala. Pasien belum pernah mengalami
kejang sebelumnya. Riwayat nyeri kepala kronik progresif maupun gangguan perilaku
sebelumnya disangkal. Dari riwayat penyakit sebelumnya pasien diketahui menderita penyakit
kencing manis, namun tidak rutin minum obat. Riwayat penyakit seperti hipertensi, stroke,
sakit jantung, asam urat dan sakit ginjal disangkal oleh penderita. Riwayat kebiasaan merokok
dan minum alkohol disangkal..
Pada pemeriksaan fisik didapatkan pasien dalam keadaan umum berat dengan
kesadaran somnolen. Tekanan darah 120/70 mmHg, nadi 110 x/menit, reguler, isi cukup,
frekuensi nafas 22 x/menit dan suhu badan 37,2ºC, saturasi oksigen 99%. Pada pemeriksaan
kepala tidak ada jejas. Pada pemeriksaan mata tidak terdapat konjungtiva yang anemis maupun
ikterik pada sklera. Pada pemeriksaan leher tidak ditemukan adanya krepitasi dan pembesaran
kelenjar getah bening. Pada pemeriksaan dada ditemukan suara jantung 1 dan 2 normal, tidak
ditemukan adanya bising pada jantung. Pada pemeriksaan paru-paru didapatkan ronkhi pada
kedua paru. Pada pemeriksaan abdomen ditemukan permukaan abdomen datar lemas, bising
usus normal dan tidak ada pembesaran dari hepar dan lien. Pada pemeriksaan ekstremitas, tidak
ditemukan adanya edema pada keempat ekstremitas dan akral hangat.
Pada pemeriksaan neurologis, GCS E3M6V4. Pupil bulat isokor dengan diameter
kanan dan kiri 3 mm, pupil kanan dan kiri reaktif terhadap cahaya langsung dan cahaya tidak
langsung. Pada pemeriksaan tanda rangsang meningeal tidak didapatkan adanya kaku kuduk,
laseque tungkai kanan dan kiri >70 dan kernig tungkai kanan dan kiri >135. Pada pemeriksaan
saraf kranialis nervus I tidak dapat dievaluasi, pemeriksaan N II didapatkan funduskopi ODS
papil bulat, warna jingga, batas tegas, rasio aa:vv = 2:3, tidak tampak perdarahan, kesan
normal. Didapatkan kesan paresis nervus VII kiri tipe upper motorneuron. Pemeriksaan nervus
3. III, IV, V dan VI tidak ditemukan kelainan. Pada pemeriksaan status motorik didapatkan kesan
hemiparesis kiri. Tonus otot ekstremitas kiri cenderung turun. Refleks fisiologis pada bisep,
trisep, brachioradialis, patela dan Achiles kiri menurun. Refleks patologis tidak ada hoffman
tromner dan babinski group. Tidak ditemukan klonus achiles dan klonus patela. Pemeriksaan
status sensorik tidak dapat dievaluasi. Pada pemeriksaan status otonom tidak didapatkan
adanya inkontinensia urin et alvi maupun retensio uri et alvi.
Pada pemeriksaan laboratorium tanggal 16 Oktober 2018 didapatkan kadar hemoglobin
12,2 gr/dl, leukosit 17100/mm3, eritrosit 4,52x106 /µl, hematokrit 38,7%, trombosit
423.000/mm3, gula darah sesaat 696 mg/dl, ureum 118mg/dl, kreatinin 2,1 mg/dl, natrium 119
mEq/L, kalium 2,6 mEq/L, klorida 82 mEq/L. Hasil ekspertisi EKG dalam batas normal.
Pemeriksaan x-ray thorax didapatkan gambaran cor dan pulmo kesan dalam batas normal.
Pasien dilakukan pemeriksaan ct-scan kepala polos dan didapatkan kesan gambaran lesi
hipodens bercampur dengan hiperdens di regio frontoparietal sinistra dikelilingi area hipodens
perifokal luas kesan suatu massa dengan kalsifikasi, dikelilingi perifokal edema. Pasien
didiagnosis kerja dengan status epileptikus + DM tipe 2 dengan stress hiperglikemia
Gambar 1. X-ray thorax
Penatalaksanaan dengan tirah baring, elevasi kepala setinggi 30°. Oksigen 4 liter per
menit lewat nasal kanul, mobilisasi miring kiri dan kanan tiap 2 jam, pemasangan pipa
nasogaster dan kateter urine dengan persetujuan dari keluarga. Pemasangan jalur IVFD NaCl
0.9% 500 cc per 8 jam, fenitoin loading dose 900 mg dalam NaCl 0,9% 100 cc, asam folat 400
μg tiap 24 jam Pada pasien dilakukan observasi tanda vital tiap 8 jam, direncanakan konsul
penyakit dalam untuk tatalaksana diabetes melitus tipe 2. Dari penyakit dalam pasien diberikan
novorapid 50 unit dalam NaCl 0,9% 500 cc + KN 2 500 cc/24 jam + NaCl 3% 250 cc 8 tpm
makro. Pasien direncanakan untuk rawat inap dan dikonsulkan ke divisi epilepsi. Hasil dari
perekaman EEG didapatkan kesan abnormal EEG karena adanya gelombang epileptiform yang
muncul selama 1,5 menit di sentral kanan yang bersamaan dengan postur distonik fokal sisi
kiri dimana temuan ini sesuai dengan suatu fokal epilepsy.
4. Gambar 2. CT Scan kepala tanpa kontras potongan aksial
Diagnosis
Diagnosis Klinis : Kejang fokal, paresis N.VII kiri, hemiparesis kiri
Diagnosis topis : lobus sentrotemporal kanan
Diagnosis Etiologis : Epilepsi fokal simptomatik
Diagnosis Patologis : iskemi, edema
Diagnosis tambahan : Diabetes mellitus tipe 2, Hiponatremia
Prognosis
Quo ad vitam : dubia ad malam
Quo ad fungsional : dubia ad malam
Quo ad Sanational : dubia ad malam
5. PEMBAHASAN
Nonketotic hyperglycemia (NKH) is a clinical syndrome consisting of severe
hyperglycemia, hyperosmolarity, and intracellular dehydration without ketoacidosis. The exact
incidence of HHS is not known, but it is estimated to account for ,1% of hospital admissions
in patients with diabetes (1). Most cases of HHS are seen in elderly patients with type 2
diabetes; however, it has also been reported in children and young adults. Diverse neurologic
symptoms have been described in patients with NKH, including hemichorea, seizure,
hemianopsia, and coma. Hemichorea in NKH has been attributed to petechial hemorrhage or
gemistocytic accumulation in the basal ganglia, and seizures have been associated with changes
in neuronal KATP channels or decreased neuronal levels of y-aminobutyric acid.4,11
Gambar 3. Kejang pada pasien dengan hiperglikemia7
The seizures pathogenesis caused by this disease is still controversial, as some people
think that the main pathogenesis is the lack of insulin. Among the patients, insulin levels are
sufficient to inhibit the free fatty acid metabolism and the subsequent ketoacidosis, but not
enough to transport glucose into the cells High blood glucose levels increase the levels of urine
glucose, causing osmotic diuresis effect and progressive dehydration, which would in turn
increase the incidence of this disease Some people believe that the possible mechanisms
include high blood glucose, high plasma osmolality and low γ- aminobutyric acid (GABA)
levels, and low focal cerebral ischemia. Specific mechanisms also include: (1) osmotic
changes. Hyperglycemia causes significant and rapid increase of intracellular osmotic pressure,
leading to nerve cell dehydration, and changes in enzyme activity and brain cell energy
metabolism. Membrane ion pump function is impaired, causing the loss of intracellular
6. potassium and the subsequent sodium accumulation, which destroys the membrane potential
and the stability of cell depolarization, ultimately resulting in seizures (2) in vivo biochemical
changes in metabolism. Citric acid cycle is inhibited in vivo in the patients with this disease,
whereas GABA metabolism is increased, causing the increased brain energy consumption, and
the reduced seizure threshold. In contrast, seizures are less frequent in ketoacidosis patients, as
ketosis acidosis increases intracellular activities of glutamate and tryptophan decarboxylase,
leading to the increased content of brain inhibitory neurotransmitter GABA. GABA is related
to the rapid changes of synaptic sensitivities by binding to the neurons, which then increases
the permeability of chloride ions. Under such conditions, the membrane potential is maintained
at a stable resting potential level and the excitatory synaptic reactivities are weakened so that
the epilepsy is prevented. This is also an alternative way to prove that the GABA contents
decrease in NKH-related epileptic seizures patients. (3) brain cell energy deficiency. Because
of the diabetic hyperglycemia, plasma fibrinogen significantly increases, red blood cell and
platelet aggregate, and blood is in a hypercoagulable state In addition, the aggravation of
existing diabetes microcirculation and small artery hyalinization, the dysfunction of endothelial
cells, and damages of cerebral blood flow autoregulation, decrease regional cerebral blood
flow, causing hypoxic ischemic damages and functional changes in cortical cells, which are
“epilepsy cells”. Such cells are sensitive to the metabolic disorders, high blood glucose
condition especially is likely to cause seizures (4) immune abnormalities: the presence of
glutamic acid decarboxylase autoantibodies in both type 1 diabetes and epilepsy. (5) studies
suggest that NKH related seizures might be linked to the brain barrier damage caused by long-
term high blood glucose. Early recognition of the underlying hyperosmolality is mandatory to
establish the diagnosis and to avoid the unnecessary use of prophylactic antiepileptic
medications, especially given that phenytoin can worsen the hyperglycemia4,5,6
Clinical features of NKH-related epileptic seizures: (1) common in the elderly (2) with
or without a previous history of diabetes and epilepsy (3). Seizures were always accompanied
with a rapid rise in blood glucose. Plasma osmolality may be normal or slightly elevated, but
not to the diagnostic criteria for diabetes hypertonic (4) urine ketone negative (5).Seizures
could not be effectively alleviated by antiepileptic drugs alone. Application of insulin to correct
hyperglycemia and metabolic disorders ended the seizures (6) seizure-related lesions were not
detected in the head imaging tests (7). If blood glucose was under control, epilepsy did not
occur any more.5
7. Gambar 4. Lokasi Kelainan Pada EEG pada pasien kejang dengan hiperglikemia8
The focal character of the seizures described during hyperglycemia has been reported
consistently over the years. Some authors have suggested that pre-existing or acute focal
lesions such as cortical dysplasia, heterotopia, asymptomatic strokes, and areas of
encephalomalacia from previous or acute injuries are predisposing factors for focal seizures in
patients with hyperglycemia. It has also been mentioned that focal declining in arteriolar or
venous circulation provoked by thrombosis may cause focal seizures. Glucose plays a critical
role in brain functions because it represents the main source of metabolic energy generation.
Focal motor epileptic episodes may be associated with hypoglycemia and NKH; however, these
do not occur with ketotic hyperglycemia, probably because of the anticonvulsant action of
ketosis. Most published reports on diabetic hyperglycemia are concerned with non-ketotic
hyperosmolar diabetic coma accompanied by severe hyperglycemia, hyperosmolality, and
dehydration, with minimal or no ketoacidosis, a severe condition which represents one extreme
of a biochemical continuum. In practice, actually, diabetics show a spectrum of hyperglycemia
and they are often detected before the development of severe hyperosmolarity. Although
occipital focal seizures have also been described , the clinical features of focal seizures in NKH
are usually those of frontal lobe epilepsy . The explanation of this condition by hyperglycemia
alone is unsatisfactory, because seizures are rare in diabetic ketoacidosis. It was hypothesized
that hyperglycemia leads to a decrease in epileptic seizure threshold by increasing metabolism
of GABA and accordingly decreasing the level of GABA, so resulting in a reduction in the
seizure threshold. 1,8
Singh and Strobos reported 21 patients where the first clinical manifestation was
epilepsia partialis continua. In this series almost all the patients had structural lesions. Seizure
types described in patients with hyperglycemia are diverse including epilepsia partialis
8. continua, which is the most frequent type, simple or complex partial seizures and less common
recognized symptoms are apnea, somatosensory symptoms, aphasia, and visual disturbance.
Seizures are less common in ketotic compared to non-ketotic hyperglycemia. Potential
explanation is that ketoacidosis decreases neuronal excitability by increasing levels of GABA
via activation of glutamic acid decarboxylase, increased cellular concentration of glutamic acid
and decreased GABA shunt. Other than changes in GABA, KATP channels have been recently
shown to be important in hyperglycemia-induced seizures. KATP channels are well known for
their action in pancreatic cells, where an increase in intracellular ATP/ADP ratio leads to
closure of the channels preventing potassium efflux leading to cell membrane depolarization
and insulin secretion.1,9
The modern definition and diagnostic criteria of HHS derived from case series reported
by Gerich et al. and Arieff and Carroll in 1971. They also provided insights into the
pathophysiology of the syndrome they called “hyperglycemic hyperosmolar nonketotic coma”
(HHNK). Arieff and Carroll’s diagnostic criteria included a blood glucose level .600 mg/dL, a
total serum osmolarity level .350 mOsm/L, and a serum acetone reaction from 0 to 2 pluses
when the serum was diluted 1:1 with water . Current diagnostic criteria of HHS recommended
by the American Diabetes Association (ADA) and international guidelines include a plasma
glucose level .600 mg/dL, plasma effective osmolarity .320 mOsm/L, and an absence of
significant ketoacidosis. The term HHNK was replaced with “hyperglycemic hyperosmolar
state” to reflect the fact that many patients present without significant decline in the level of
consciousness (less than one-third of patients present with coma) and because many patients
can present with mild to moderate degrees of ketosis (32,60). In some studies, up to 20% of
patients with severe hyperglycemia and hyperosmolarity were reported to have combined
features of HHS and DKA11,12,13
9. Tabel 1. Kriteria Diagnosis Hiperglikemi Hiperosmolar Non Ketotik
Once newly epileptic seizure was diagnosed, antiepileptic treatment was immediately
conducted. Intramuscular administration of phenobarbital, diazepam and valproate, or
valproate combined with carbamazepine was applied in defined cases, but with suboptimal
results. After blood glucose levels increased, insulin infusion or subcutaneous injection were
immediate applied. Close monitoring of blood glucose, saline rehydration and aggressiveness
simultaneously corrected acid-base unbalance and water and electrolyte disorders. If blood
glucose levels dropped to 8-15 mmol/L and epileptic episodes stopped, the antiepileptic drugs
would be discontinued.5
Primary treatment for the NKH-related epileptic seizures included early, active, and
rational rehydration and insulin hypoglycemic therapy, while closely monitoring blood
glucose. Such treatments are key to the success of salvage therapy among these patients.
Phenytoin-induced insulin resistance can inhibit the release of insulin, and therefore increase
the possibility of NKH-related seizures. Diazepam increase the opening frequency of GABA-
mediated chloride ion channel. Phenobarbital extended the start time of GABA-mediated
chloride channel, by reducing the brain GABA levels among the patients with NKH-related
seizures, Therefore, the stability and antiepileptic effects of phenobarbital and Diazepam
decline which explained why conventional antiepileptic drugs in those patients with epilepsy
were not marketly effective. Antiepileptic drugs preferred include carbamazepine, clonazepam
diazepam and other anti-epileptic drugs as they do not affect the levels of blood glucose. Long-
term use of anti-epileptic drugs is not necessary. If blood glucose and the seizures are well
controlled, anti-epileptic drugs can be discontinued gradually.5,10
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hyperglycemia: clinical and biochemical profile of 21 patients. Ann Neurol
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