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73 Cards in this Set
- Front
- Back
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The diagnosis of hypertensive encephalopathy is established when lowering the blood pressure results in rapid resolution of symptoms. This is accomplished with
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sodium nitroprusside, Alternative approaches include diazoxide, 50-100 mg by intravenous bolus every 5-10 minutes (to a maximum of 600 mg) or 10-30 mg/min by constant intravenous infusion, or labetalol
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The diagnosis of hypertensive encephalopathy is established when lowering the blood pressure results in rapid resolution of symptoms. This is accomplished with
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sodium nitroprusside, Alternative approaches include diazoxide, 50-100 mg by intravenous bolus every 5-10 minutes (to a maximum of 600 mg) or 10-30 mg/min by constant intravenous infusion, or labetalol
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TTP cause
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the cause is an autoimmune reaction against the metalloprotease ADAMTS13, which allows multimers of von Willebrand factor to accumulate in the plasma, where they stimulate platelet aggregation
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TTP cause
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the cause is an autoimmune reaction against the metalloprotease ADAMTS13, which allows multimers of von Willebrand factor to accumulate in the plasma, where they stimulate platelet aggregation
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TTP cause
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the cause is an autoimmune reaction against the metalloprotease ADAMTS13, which allows multimers of von Willebrand factor to accumulate in the plasma, where they stimulate platelet aggregation
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Concussion is characterized by
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transient loss of consciousness for seconds to minutes without demonstrable structural defects
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Concussion is characterized by
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transient loss of consciousness for seconds to minutes without demonstrable structural defects
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Concussion is characterized by
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transient loss of consciousness for seconds to minutes without demonstrable structural defects
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Intracerebral contusion (bruising) or hemorrhage related to head injury is usually located
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located at the frontal or temporal poles. Blood typically enters the CSF, resulting in signs of meningeal irritation and sometimes hydrocephalus. Focal neurologic signs are usually absent or subtle.
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Intracerebral contusion (bruising) or hemorrhage related to head injury is usually located
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located at the frontal or temporal poles. Blood typically enters the CSF, resulting in signs of meningeal irritation and sometimes hydrocephalus. Focal neurologic signs are usually absent or subtle.
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Epidural hematoma tends to appear as a
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biconvex, lens-shaped, extra-axial mass that may cross the midline or the tentorium but not the cranial sutures
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Epidural hematoma tends to appear as a
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biconvex, lens-shaped, extra-axial mass that may cross the midline or the tentorium but not the cranial sutures
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Epidural hematoma tends to appear as a
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biconvex, lens-shaped, extra-axial mass that may cross the midline or the tentorium but not the cranial sutures
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biconvex, lens-shaped, extra-axial mass that may cross the midline or the tentorium but not the cranial sutures
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Epidural hematoma tends to appear as a
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biconvex, lens-shaped, extra-axial mass that may cross the midline or the tentorium but not the cranial sutures
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Epidural hematoma tends to appear as a
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crescent-shaped and may cross the cranial sutures but not the midline or tentorium
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Subdural hematoma
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crescent-shaped and may cross the cranial sutures but not the midline or tentorium
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Subdural hematoma
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crescent-shaped and may cross the cranial sutures but not the midline or tentorium
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Subdural hematoma
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crescent-shaped and may cross the cranial sutures but not the midline or tentorium
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Subdural hematoma
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hen postictal confusion does not clear rapidly, an explanation for the prolonged postictal state must be sought. This occurs in three settings
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status epilepticus, an underlying structural brain abnormality (e.g., stroke, intracranial hemorrhage), and an underlying diffuse cerebral disorder (e.g., dementia, meningitis or encephalitis, metabolic encephalopathy).
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hen postictal confusion does not clear rapidly, an explanation for the prolonged postictal state must be sought. This occurs in three settings
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status epilepticus, an underlying structural brain abnormality (e.g., stroke, intracranial hemorrhage), and an underlying diffuse cerebral disorder (e.g., dementia, meningitis or encephalitis, metabolic encephalopathy).
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hen postictal confusion does not clear rapidly, an explanation for the prolonged postictal state must be sought. This occurs in three settings
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status epilepticus, an underlying structural brain abnormality (e.g., stroke, intracranial hemorrhage), and an underlying diffuse cerebral disorder (e.g., dementia, meningitis or encephalitis, metabolic encephalopathy).
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hen postictal confusion does not clear rapidly, an explanation for the prolonged postictal state must be sought. This occurs in three settings
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status epilepticus, an underlying structural brain abnormality (e.g., stroke, intracranial hemorrhage), and an underlying diffuse cerebral disorder (e.g., dementia, meningitis or encephalitis, metabolic encephalopathy).
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intracellular deposits containing hyperphosphorylated tau (a microtubule-associated protein) and ubiquitin.
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Neurofibrillary tangles
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intracellular deposits containing hyperphosphorylated tau (a microtubule-associated protein) and ubiquitin.
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Neurofibrillary tangles
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intracellular deposits containing hyperphosphorylated tau (a microtubule-associated protein) and ubiquitin.
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Neurofibrillary tangles
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In other kindreds, familial Alzheimer disease has an especially early onset and more virulent course and is linked to mutations in the gene for
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presenilin 1, a transmembrane protein, on chromosome 14.
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In other kindreds, familial Alzheimer disease has an especially early onset and more virulent course and is linked to mutations in the gene for
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presenilin 1, a transmembrane protein, on chromosome 14.
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In late-onset familial (and to a lesser extent sporadic) Alzheimer disease, the risk of being affected and the age at onset are related to the number
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related to the number of apolipoprotein E e-4 (APOE4) alleles on chromosome 19.
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In late-onset familial (and to a lesser extent sporadic) Alzheimer disease, the risk of being affected and the age at onset are related to the number
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related to the number of apolipoprotein E e-4 (APOE4) alleles on chromosome 19.
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principal constituent of neuritic plaques
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b-amyloid
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principal constituent of neuritic plaques
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b-amyloid
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principal constituent of neuritic plaques
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b-amyloid
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frontal lobe gait
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frontal lobe gait disorder may become apparent, with short, slow, shuffling steps, flexed posture, wide base, and difficulty in initiating walking
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frontal lobe gait
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frontal lobe gait disorder may become apparent, with short, slow, shuffling steps, flexed posture, wide base, and difficulty in initiating walking
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frontal lobe gait
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frontal lobe gait disorder may become apparent, with short, slow, shuffling steps, flexed posture, wide base, and difficulty in initiating walking
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Histopathologic findings include tau- or ubiquitin-containing inclusions
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FRONTOTEMPORAL DEMENTIA
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Histopathologic findings include tau- or ubiquitin-containing inclusions
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FRONTOTEMPORAL DEMENTIA
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FRONTOTEMPORAL DEMENTIA
When the nondominant temporal lobe is affected primarily, patients may present with |
prosopagnosia, an inability to recognize faces
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FRONTOTEMPORAL DEMENTIA
When the nondominant temporal lobe is affected primarily, patients may present with |
prosopagnosia, an inability to recognize faces
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Clinical features of sporadic Creutzfeldt-Jakob disease.]
Aside from cognitive abnormalities, the most frequent clinical manifestations |
myoclonus (often induced by a startle), extrapyramidal signs (rigidity, bradykinesia, tremor, dystonia, chorea, or athetosis), cerebellar signs, and extrapyramidal signs. Visual field defects, cranial nerve palsies, and seizures occur less often.
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Clinical features of sporadic Creutzfeldt-Jakob disease.]
Aside from cognitive abnormalities, the most frequent clinical manifestations |
myoclonus (often induced by a startle), extrapyramidal signs (rigidity, bradykinesia, tremor, dystonia, chorea, or athetosis), cerebellar signs, and extrapyramidal signs. Visual field defects, cranial nerve palsies, and seizures occur less often.
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Clinical features of sporadic Creutzfeldt-Jakob disease.]
Aside from cognitive abnormalities, the most frequent clinical manifestations |
myoclonus (often induced by a startle), extrapyramidal signs (rigidity, bradykinesia, tremor, dystonia, chorea, or athetosis), cerebellar signs, and extrapyramidal signs. Visual field defects, cranial nerve palsies, and seizures occur less often.
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The EEG may show periodic sharp waves or spikes
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Creutzfeldt-Jakob disease
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The EEG may show periodic sharp waves or spikes
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Creutzfeldt-Jakob disease
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The EEG may show periodic sharp waves or spikes
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Creutzfeldt-Jakob disease
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Diffusion-weighted image of the brain in Creutzfeldt-Jakob disease, showing characteristic
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hyperintensities (white) in the basal ganglia and cortical ribbon (A), and EEG with typical triphasic waves in all leads (B), which occur repetitively about once every second.]
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Diffusion-weighted image of the brain in Creutzfeldt-Jakob disease, showing characteristic
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hyperintensities (white) in the basal ganglia and cortical ribbon (A), and EEG with typical triphasic waves in all leads (B), which occur repetitively about once every second.]
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Diffusion-weighted image of the brain in Creutzfeldt-Jakob disease, showing characteristic
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hyperintensities (white) in the basal ganglia and cortical ribbon (A), and EEG with typical triphasic waves in all leads (B), which occur repetitively about once every second.]
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Diffusion-weighted image of the brain in Creutzfeldt-Jakob disease, showing characteristic
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hyperintensities (white) in the basal ganglia and cortical ribbon (A), and EEG with typical triphasic waves in all leads (B), which occur repetitively about once every second.]
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Diffusion-weighted image of the brain in Creutzfeldt-Jakob disease, showing characteristic
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hyperintensities (white) in the basal ganglia and cortical ribbon (A), and EEG with typical triphasic waves in all leads (B), which occur repetitively about once every second.]
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Circulation of cerebrospinal fluid (CSF).
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CSF is produced by the choroid plexus, which consists of specialized secretory tissue located within the cerebral ventricles. It flows from the lateral and third ventricles through the cerebral aqueduct and fourth ventricle and exits the ventricular system through two laterally situated foramina of Luschka and a single, medially located foramen of Magendie. CSF then enters and circulates through the subarachnoid space surrounding the brain and spinal cord. It is ultimately absorbed through arachnoid granulations into the venous circulation.0
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Circulation of cerebrospinal fluid (CSF).
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CSF is produced by the choroid plexus, which consists of specialized secretory tissue located within the cerebral ventricles. It flows from the lateral and third ventricles through the cerebral aqueduct and fourth ventricle and exits the ventricular system through two laterally situated foramina of Luschka and a single, medially located foramen of Magendie. CSF then enters and circulates through the subarachnoid space surrounding the brain and spinal cord. It is ultimately absorbed through arachnoid granulations into the venous circulation.0
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Circulation of cerebrospinal fluid (CSF).
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CSF is produced by the choroid plexus, which consists of specialized secretory tissue located within the cerebral ventricles. It flows from the lateral and third ventricles through the cerebral aqueduct and fourth ventricle and exits the ventricular system through two laterally situated foramina of Luschka and a single, medially located foramen of Magendie. CSF then enters and circulates through the subarachnoid space surrounding the brain and spinal cord. It is ultimately absorbed through arachnoid granulations into the venous circulation.0
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Circulation of cerebrospinal fluid (CSF).
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CSF is produced by the choroid plexus, which consists of specialized secretory tissue located within the cerebral ventricles. It flows from the lateral and third ventricles through the cerebral aqueduct and fourth ventricle and exits the ventricular system through two laterally situated foramina of Luschka and a single, medially located foramen of Magendie. CSF then enters and circulates through the subarachnoid space surrounding the brain and spinal cord. It is ultimately absorbed through arachnoid granulations into the venous circulation.0
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Circulation of cerebrospinal fluid (CSF).
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CSF is produced by the choroid plexus, which consists of specialized secretory tissue located within the cerebral ventricles. It flows from the lateral and third ventricles through the cerebral aqueduct and fourth ventricle and exits the ventricular system through two laterally situated foramina of Luschka and a single, medially located foramen of Magendie. CSF then enters and circulates through the subarachnoid space surrounding the brain and spinal cord. It is ultimately absorbed through arachnoid granulations into the venous circulation.0
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round, eosinophilic, intracytoplasmic neuronal inclusions
These contain a-synuclein |
Lewy bodies
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round, eosinophilic, intracytoplasmic neuronal inclusions
These contain a-synuclein |
Lewy bodies
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round, eosinophilic, intracytoplasmic neuronal inclusions
These contain a-synuclein |
Lewy bodies
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round, eosinophilic, intracytoplasmic neuronal inclusions
These contain a-synuclein |
Lewy bodies
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round, eosinophilic, intracytoplasmic neuronal inclusions
These contain a-synuclein |
Lewy bodies
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characterize Lewy body dementia
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it is characterized clinically by cognitive decline without prominent early memory impairment. Other distinctive features include fluctuating cognitive ability, well-formed visual hallucinations, and signs of parkinsonism, especially rigidity and bradykinesia. These patients may respond well to anticholinesterase drugs such as tacrine or donepezil (Table 1-25), but are especially sensitive to extrapyramidal side effects of antipsychotic drugs, which therefore should be avoided or used with caution
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characterize Lewy body dementia
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it is characterized clinically by cognitive decline without prominent early memory impairment. Other distinctive features include fluctuating cognitive ability, well-formed visual hallucinations, and signs of parkinsonism, especially rigidity and bradykinesia. These patients may respond well to anticholinesterase drugs such as tacrine or donepezil (Table 1-25), but are especially sensitive to extrapyramidal side effects of antipsychotic drugs, which therefore should be avoided or used with caution
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characterize Lewy body dementia
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it is characterized clinically by cognitive decline without prominent early memory impairment. Other distinctive features include fluctuating cognitive ability, well-formed visual hallucinations, and signs of parkinsonism, especially rigidity and bradykinesia. These patients may respond well to anticholinesterase drugs such as tacrine or donepezil (Table 1-25), but are especially sensitive to extrapyramidal side effects of antipsychotic drugs, which therefore should be avoided or used with caution
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characterize Lewy body dementia
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it is characterized clinically by cognitive decline without prominent early memory impairment. Other distinctive features include fluctuating cognitive ability, well-formed visual hallucinations, and signs of parkinsonism, especially rigidity and bradykinesia. These patients may respond well to anticholinesterase drugs such as tacrine or donepezil (Table 1-25), but are especially sensitive to extrapyramidal side effects of antipsychotic drugs, which therefore should be avoided or used with caution
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characterize Lewy body dementia
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it is characterized clinically by cognitive decline without prominent early memory impairment. Other distinctive features include fluctuating cognitive ability, well-formed visual hallucinations, and signs of parkinsonism, especially rigidity and bradykinesia. These patients may respond well to anticholinesterase drugs such as tacrine or donepezil (Table 1-25), but are especially sensitive to extrapyramidal side effects of antipsychotic drugs, which therefore should be avoided or used with caution
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PROGRESSIVE SUPRANUCLEAR PALSY description
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Progressive supranuclear palsy is an idiopathic degenerative disorder that primarily affects subcortical gray matter regions of the brain. The classic clinical features are supranuclear ophthalmoplegia, pseudobulbar palsy, axial dystonia with or without extrapyramidal rigidity of the limbs, and dementia
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PROGRESSIVE SUPRANUCLEAR PALSY description
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Progressive supranuclear palsy is an idiopathic degenerative disorder that primarily affects subcortical gray matter regions of the brain. The classic clinical features are supranuclear ophthalmoplegia, pseudobulbar palsy, axial dystonia with or without extrapyramidal rigidity of the limbs, and dementia
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PROGRESSIVE SUPRANUCLEAR PALSY description
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Progressive supranuclear palsy is an idiopathic degenerative disorder that primarily affects subcortical gray matter regions of the brain. The classic clinical features are supranuclear ophthalmoplegia, pseudobulbar palsy, axial dystonia with or without extrapyramidal rigidity of the limbs, and dementia
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General paresis characterized by...
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chronic meningoencephalitis caused by active spirochetal infection, this was the usual cause of dementia and psychiatric disorders related to neurosyphilis in the prepenicillin era. Onset is with gradual memory loss or altered affect, personality, or behavior. This is followed by global intellectual deterioration with grandiosity, depression, psychosis, and focal weakness. Terminal features include incontinence, seizures, or strokes. Neurologic examination may show tremor of the face and tongue, paucity of facial expression, dysarthria, and pyramidal signs
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General paresis characterized by...
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chronic meningoencephalitis caused by active spirochetal infection, this was the usual cause of dementia and psychiatric disorders related to neurosyphilis in the prepenicillin era. Onset is with gradual memory loss or altered affect, personality, or behavior. This is followed by global intellectual deterioration with grandiosity, depression, psychosis, and focal weakness. Terminal features include incontinence, seizures, or strokes. Neurologic examination may show tremor of the face and tongue, paucity of facial expression, dysarthria, and pyramidal signs
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General paresis characterized by...
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chronic meningoencephalitis caused by active spirochetal infection, this was the usual cause of dementia and psychiatric disorders related to neurosyphilis in the prepenicillin era. Onset is with gradual memory loss or altered affect, personality, or behavior. This is followed by global intellectual deterioration with grandiosity, depression, psychosis, and focal weakness. Terminal features include incontinence, seizures, or strokes. Neurologic examination may show tremor of the face and tongue, paucity of facial expression, dysarthria, and pyramidal signs
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General paresis characterized by...
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chronic meningoencephalitis caused by active spirochetal infection, this was the usual cause of dementia and psychiatric disorders related to neurosyphilis in the prepenicillin era. Onset is with gradual memory loss or altered affect, personality, or behavior. This is followed by global intellectual deterioration with grandiosity, depression, psychosis, and focal weakness. Terminal features include incontinence, seizures, or strokes. Neurologic examination may show tremor of the face and tongue, paucity of facial expression, dysarthria, and pyramidal signs
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