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Pathology - Syringomyelia
Commonly linked to Arnold-Chiari malformation or thoracic kyphoscoliosis; can also result from intraspinal neoplasms or trauma.
A fluid-filled hollow typically forms in the spinal cord, often extending from the central canal, mainly in the cervical area (most commonly C7-T1). This leads to the loss of nearby gray and white matter, including the crossing fibers of the spinothalamic tract, resulting in reactive gliosis.
Loss of pain and temperature feeling in the upper extremities typically accompanied by intact touch and proprioception; may later extend to affect motor and other sensory pathways.
Treatment
Surgical drainage of a cavity.
Commonly linked to Arnold-Chiari malformation or thoracic kyphoscoliosis; can also result from intraspinal neoplasms or trauma.
A fluid-filled hollow typically forms in the spinal cord, often extending from the central canal, mainly in the cervical area (most commonly C7-T1). This leads to the loss of nearby gray and white matter, including the crossing fibers of the spinothalamic tract, resulting in reactive gliosis.
Loss of pain and temperature feeling in the upper extremities typically accompanied by intact touch and proprioception; may later extend to affect motor and other sensory pathways.
Treatment
Surgical drainage of a cavity.
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Pathology - Myasthenia Gravis
Resulting from antibodies targeting the acetylcholine receptors at the neuromuscular junction.
Linked to thymoma, thymic hyperplasia, or other autoimmune diseases.
Most commonly occurs in women under 40 years old.
Neuromuscular junction is affected by a decrease in acetylcholine receptors and the presence of immune complexes and complement factors.
Pathophysiology: Antibodies cause degradation of acetylcholine receptors, resulting in a near-complete inhibition of synaptic transmission.
Initial symptoms often include ptosis or diplopia caused by extraocular muscle weakness, which can progress with exhaustion. Other often affected muscles, such as those in the extremities or face, may also experience easy tiredness.
Diagnosis was verified through improvement following the injection of a short-acting anticholinesterase (edrophonium).
Laboratory results: Presence of antibodies targeting cholinergic receptors.
Treatment includes anticholinesterase medications such as pyridostigmine, thymectomy, immunosuppression, and plasmapheresis in cases of severe flare.
Resulting from antibodies targeting the acetylcholine receptors at the neuromuscular junction.
Linked to thymoma, thymic hyperplasia, or other autoimmune diseases.
Most commonly occurs in women under 40 years old.
Neuromuscular junction is affected by a decrease in acetylcholine receptors and the presence of immune complexes and complement factors.
Pathophysiology: Antibodies cause degradation of acetylcholine receptors, resulting in a near-complete inhibition of synaptic transmission.
Initial symptoms often include ptosis or diplopia caused by extraocular muscle weakness, which can progress with exhaustion. Other often affected muscles, such as those in the extremities or face, may also experience easy tiredness.
Diagnosis was verified through improvement following the injection of a short-acting anticholinesterase (edrophonium).
Laboratory results: Presence of antibodies targeting cholinergic receptors.
Treatment includes anticholinesterase medications such as pyridostigmine, thymectomy, immunosuppression, and plasmapheresis in cases of severe flare.
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Pathology-Seizures
Seizures can be caused by toxins (such as drugs or alcohol withdrawal), intracranial issues (including stroke, bleeding, tumors, infections, or degenerative disorders), metabolic imbalances (such as low sodium or low blood sugar), or epilepsy (a condition characterized by recurring seizures).
Neurologic symptoms occur due to abnormal discharge of central nervous system neurons.
The seizure is typically preceded by an aura, which might involve unusual smells or visual disturbances, and is then followed by the seizure itself. There is generally a postictal interval after the seizure, characterized by minutes to hours of bewilderment and tiredness.
Seizures can be categorized as either partial, affecting a specific area of the brain, or generalized. Simple partial seizures do not result in a loss of consciousness and can affect motor, sensory, or autonomic functions of the brain. (2) Complex partial seizures are similar to simple partial seizures, but they involve compromised consciousness. (3) Tonic-clonic (grand mal): muscular contractions alternating with relaxation;
(4) Absence: temporary loss of awareness without losing muscle control; (5) Myoclonic: abrupt, short muscle contractions.
Therapy
Anticonvulsant medications; address root issues.
Status epilepticus is defined as a prolonged tonic-clonic seizure lasting more than 30 minutes.
Possible complications involve anoxic brain damage and lactic acidosis.
Seizures can be caused by toxins (such as drugs or alcohol withdrawal), intracranial issues (including stroke, bleeding, tumors, infections, or degenerative disorders), metabolic imbalances (such as low sodium or low blood sugar), or epilepsy (a condition characterized by recurring seizures).
Neurologic symptoms occur due to abnormal discharge of central nervous system neurons.
The seizure is typically preceded by an aura, which might involve unusual smells or visual disturbances, and is then followed by the seizure itself. There is generally a postictal interval after the seizure, characterized by minutes to hours of bewilderment and tiredness.
Seizures can be categorized as either partial, affecting a specific area of the brain, or generalized. Simple partial seizures do not result in a loss of consciousness and can affect motor, sensory, or autonomic functions of the brain. (2) Complex partial seizures are similar to simple partial seizures, but they involve compromised consciousness. (3) Tonic-clonic (grand mal): muscular contractions alternating with relaxation;
(4) Absence: temporary loss of awareness without losing muscle control; (5) Myoclonic: abrupt, short muscle contractions.
Therapy
Anticonvulsant medications; address root issues.
Status epilepticus is defined as a prolonged tonic-clonic seizure lasting more than 30 minutes.
Possible complications involve anoxic brain damage and lactic acidosis.
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Pathology-Meningitis
Pyogenic meningitis is caused by different bacteria depending on the age group: Group B streptococci, Escherichia coli, and Listeria in neonates and infants; Haemophilus influenzae and Neisseria meningitidis in children and young adults; and pneumococcus, Listeria, and gram-negative rods in older individuals.
Causes of viral meningitis include HSY virus, Coxsackievirus, echoviruses, and arboviruses.
Pyogenic meningitis is characterized by a purulent discharge in the leptomeninges, engorged meningeal arteries, and the presence of neutrophils in the subarachnoid space.
Viral meningitis may show either no abnormalities or a slight lymphocytic infiltration in the subarachnoid space, with moderate edema perhaps occurring.
Pyogenic meningitis presents with symptoms such as headache, photophobia, neck stiffness, fever, and altered mental status.
Laboratory results indicate that the cerebrospinal fluid obtained from a lumbar puncture appears cloudy, contains neutrophils, has elevated protein levels, reduced glucose levels, and demonstrates increased opening pressure.
Symptoms of viral meningitis include headache, photophobia, neck stiffness, fever, and altered mental status. Lab results: Lumbar puncture indicates an increase in lymphocytes, slightly raised protein levels, and normal glucose levels.
Pyogenic meningitis is treated with antibiotics and supportive care. Steroids may be considered for H influenzae infection.
Viral meningitis is a self-limiting condition. Acyclovir is used for herpes simplex virus (HSY) meningitis.
Viral encephalitis is an infection that affects the brain and/or meninges.
It can be caused by several organisms such as arboviruses, herpes, CMY, rabies, and poliovirus.
Glial nodules, neuronal inclusion bodies, and perivascular mononuclear cell infiltrates are observed histopathologically.
Pyogenic meningitis is caused by different bacteria depending on the age group: Group B streptococci, Escherichia coli, and Listeria in neonates and infants; Haemophilus influenzae and Neisseria meningitidis in children and young adults; and pneumococcus, Listeria, and gram-negative rods in older individuals.
Causes of viral meningitis include HSY virus, Coxsackievirus, echoviruses, and arboviruses.
Pyogenic meningitis is characterized by a purulent discharge in the leptomeninges, engorged meningeal arteries, and the presence of neutrophils in the subarachnoid space.
Viral meningitis may show either no abnormalities or a slight lymphocytic infiltration in the subarachnoid space, with moderate edema perhaps occurring.
Pyogenic meningitis presents with symptoms such as headache, photophobia, neck stiffness, fever, and altered mental status.
Laboratory results indicate that the cerebrospinal fluid obtained from a lumbar puncture appears cloudy, contains neutrophils, has elevated protein levels, reduced glucose levels, and demonstrates increased opening pressure.
Symptoms of viral meningitis include headache, photophobia, neck stiffness, fever, and altered mental status. Lab results: Lumbar puncture indicates an increase in lymphocytes, slightly raised protein levels, and normal glucose levels.
Pyogenic meningitis is treated with antibiotics and supportive care. Steroids may be considered for H influenzae infection.
Viral meningitis is a self-limiting condition. Acyclovir is used for herpes simplex virus (HSY) meningitis.
Viral encephalitis is an infection that affects the brain and/or meninges.
It can be caused by several organisms such as arboviruses, herpes, CMY, rabies, and poliovirus.
Glial nodules, neuronal inclusion bodies, and perivascular mononuclear cell infiltrates are observed histopathologically.
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Pathology- Bell Palsy
The precise cause is uncertain, however it is believed to be related to viral reactivation, particularly by HSV-1 or herpes zoster virus, as well as inflammatory and immunological factors.
Most commonly occurs in adults, diabetics, or during pregnancy.
Study of the disordered physiological processes that cause disease.
Edema and inflammation cause compression of the facial nerve in the temporal bone canal, where the nerve passes through.
Clinical Symptoms and Signs
The sudden onset of paralysis in the upper and lower face, reduced taste sensation, ear pain on the same side, drooling, dry eyes with reduced tear production, and potential corneal injury (infection or ulceration) caused by the inability to fully seal the affected eye.
Therapy
Consider using corticosteroids and antiviral medication (acyclovir) to manage the condition. Additionally, provide eye care by using ocular lubrication to reduce the chances of corneal damage.
The prognosis is favorable, with 80%-90% of patients achieving full recovery within 6-12 weeks.
The precise cause is uncertain, however it is believed to be related to viral reactivation, particularly by HSV-1 or herpes zoster virus, as well as inflammatory and immunological factors.
Most commonly occurs in adults, diabetics, or during pregnancy.
Study of the disordered physiological processes that cause disease.
Edema and inflammation cause compression of the facial nerve in the temporal bone canal, where the nerve passes through.
Clinical Symptoms and Signs
The sudden onset of paralysis in the upper and lower face, reduced taste sensation, ear pain on the same side, drooling, dry eyes with reduced tear production, and potential corneal injury (infection or ulceration) caused by the inability to fully seal the affected eye.
Therapy
Consider using corticosteroids and antiviral medication (acyclovir) to manage the condition. Additionally, provide eye care by using ocular lubrication to reduce the chances of corneal damage.
The prognosis is favorable, with 80%-90% of patients achieving full recovery within 6-12 weeks.
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Pathology- Retinoblastoma
A tumor suppressor gene called RB found on chromosome 13 is deleted in both alleles, resulting in a tumor originating from neuroepithelial cells in the retina. Can be hereditary or random. The familial form is inherited as an autosomal dominant characteristic, requiring homozygosity for disease manifestation. Over 90% of those who are heterozygous carriers ultimately get the condition.
The retina consists of circular cells with darkly stained nuclei and little cytoplasm organized in Flexner-Wintersteiner rosettes (cuboidal cells surrounding a central lumen).
Can spread to the brain, spinal cord, bone, or lymph nodes.
Medical Typically seen in young children (familial form) who display reduced visual acuity, eye discomfort, strabismus, intraocular mass on funduscopic examination, and white cat's eye pupillary reflex.
Individuals with familial disease are prone to getting retinoblastoma in both eyes and have a heightened susceptibility to other malignancies such as osteosarcoma.
Surgical excision of tumor or eye if required, followed by radiation therapy.
A tumor becomes lethal after it has metastasized beyond the eye.
Notes Knudson's two-hit hypothesis prototype: Two mutations are necessary for the disease to occur. Deletion can be either hereditary (familial) or sporadic. The second mutation arises sporadically in both familial and sporadic instances.
A tumor suppressor gene called RB found on chromosome 13 is deleted in both alleles, resulting in a tumor originating from neuroepithelial cells in the retina. Can be hereditary or random. The familial form is inherited as an autosomal dominant characteristic, requiring homozygosity for disease manifestation. Over 90% of those who are heterozygous carriers ultimately get the condition.
The retina consists of circular cells with darkly stained nuclei and little cytoplasm organized in Flexner-Wintersteiner rosettes (cuboidal cells surrounding a central lumen).
Can spread to the brain, spinal cord, bone, or lymph nodes.
Medical Typically seen in young children (familial form) who display reduced visual acuity, eye discomfort, strabismus, intraocular mass on funduscopic examination, and white cat's eye pupillary reflex.
Individuals with familial disease are prone to getting retinoblastoma in both eyes and have a heightened susceptibility to other malignancies such as osteosarcoma.
Surgical excision of tumor or eye if required, followed by radiation therapy.
A tumor becomes lethal after it has metastasized beyond the eye.
Notes Knudson's two-hit hypothesis prototype: Two mutations are necessary for the disease to occur. Deletion can be either hereditary (familial) or sporadic. The second mutation arises sporadically in both familial and sporadic instances.
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Pathology - Glioblastoma Multiforme
Linked to genetic alterations in many oncogenes and tumor suppressor genes, such as p53 and the RB gene.
Most prevalent primary brain tumor.
Most commonly found in individuals aged 40 to 60.
Pathology: Irregular, unconfined lesion located in the cerebral hemisphere.
Microscopic examination reveals a high-grade astrocytoma originating from astrocytes. Central regions show necrosis and bleeding surrounding by many tumor cells grouped in a pseudopalisading pattern, displaying a high level of anaplasia.
Symptoms and signs
Seizures, headaches, nausea, vomiting, and other symptoms indicating elevated intracranial pressure.
Imaging shows mass effect and cerebral edema caused by a tumor.
Treatments: Surgical excision along with chemotherapy and radiation therapy.
The prognosis is very grim, with the majority of patients succumbing within a year of being diagnosed.
Benign low-grade astrocytomas, particularly pilocytic astrocytomas, are slow-growing tumors seen in the cerebellum of children. Rosenthal fibers, which are eosinophilic corkscrew fibers, are observed on histological examination.
Linked to genetic alterations in many oncogenes and tumor suppressor genes, such as p53 and the RB gene.
Most prevalent primary brain tumor.
Most commonly found in individuals aged 40 to 60.
Pathology: Irregular, unconfined lesion located in the cerebral hemisphere.
Microscopic examination reveals a high-grade astrocytoma originating from astrocytes. Central regions show necrosis and bleeding surrounding by many tumor cells grouped in a pseudopalisading pattern, displaying a high level of anaplasia.
Symptoms and signs
Seizures, headaches, nausea, vomiting, and other symptoms indicating elevated intracranial pressure.
Imaging shows mass effect and cerebral edema caused by a tumor.
Treatments: Surgical excision along with chemotherapy and radiation therapy.
The prognosis is very grim, with the majority of patients succumbing within a year of being diagnosed.
Benign low-grade astrocytomas, particularly pilocytic astrocytomas, are slow-growing tumors seen in the cerebellum of children. Rosenthal fibers, which are eosinophilic corkscrew fibers, are observed on histological examination.
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Pathology - Meningioma
Benign tumor originating from meningothelial cells of the arachnoid, located outside the brain.
Most prevalent among women over the age of 30.
Pathology: Typically a spherical encapsulated mass with a dural base, commonly found in the convexities of the cerebral hemispheres or the parasagittal area, and normally does not invade the brain.
Microscopic examination reveals a tightly packed whorled pattern of tumor cells together with psammoma masses with laminated calcifications.
Symptoms related to the compression of the underlying brain, such as seizures, headaches, nausea, vomiting, and other indications of elevated intracranial pressure.
Surgically remove the tumor if it causes symptoms.
The prognosis is favorable.
Meningiomas rank as the second most prevalent primary brain tumors.
Patients with neurofibromatosis type 2 may have several meningiomas.
Benign tumor originating from meningothelial cells of the arachnoid, located outside the brain.
Most prevalent among women over the age of 30.
Pathology: Typically a spherical encapsulated mass with a dural base, commonly found in the convexities of the cerebral hemispheres or the parasagittal area, and normally does not invade the brain.
Microscopic examination reveals a tightly packed whorled pattern of tumor cells together with psammoma masses with laminated calcifications.
Symptoms related to the compression of the underlying brain, such as seizures, headaches, nausea, vomiting, and other indications of elevated intracranial pressure.
Surgically remove the tumor if it causes symptoms.
The prognosis is favorable.
Meningiomas rank as the second most prevalent primary brain tumors.
Patients with neurofibromatosis type 2 may have several meningiomas.
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Pathology - Ischemic Stroke
Possible causes are thrombosis, embolism, dissection, vasculitis, or hypotension.
Risk factors including tobacco use, hypertension, atrial fibrillation, hyperlipidemia, and diabetes.
Cerebral infarction is linked to thrombosis or embolism and results in ischemic neuronal changes such as nuclear pyknosis and eosinophilic cytoplasm within 12 hours. Microglia and monocyte infiltration occur within 2 days, followed by liquefactive necrosis leading to a fluid-filled cavity and reactive astrocytes within 1-3 weeks. Gliosis, which is scar formation, can occur after several months and the infarction may progress to hemorrhagic infarction.
Watershed infarction is linked to low blood pressure and manifests as a wedge-shaped infarction at the border of the artery's supply area, typically found between the distribution of the anterior cerebral artery (ACA) and middle cerebral artery (MCA).
Lacunar infarcts are linked to high blood pressure and blockage of small blood vessels due to blood clots, resulting in small empty spaces surrounded by scar tissue in the brain.
It varies based on the location of reduced blood flow and the degree of alternative blood supply.
Anterior Cerebral Artery (ACA): Contralateral leg weakness and sensory loss.
Middle Cerebral Artery (MCA) presents with contralateral paralysis, sensory loss, contralateral hemianopia, and aphasias.
Proximal Cerebral Artery (PCA) symptoms include contralateral sensory disruption and homonymous hemianopia, with or without macular-sparing.
Damage to the lateral striate arteries results in contralateral paralysis.
Administer thrombolytic therapy after 4.5 hours of symptom onset if no signs of hemorrhage. Use antiplatelet medication such as aspirin and dipyridamole. Modify risk factors by treating hypertension and hyperlipidemia.
A transient ischemic attack is a temporary episode of neurological symptoms resulting from reduced blood flow to the brain, which typically lasts less than 24 hours and indicates a high risk of a future stroke.
Possible causes are thrombosis, embolism, dissection, vasculitis, or hypotension.
Risk factors including tobacco use, hypertension, atrial fibrillation, hyperlipidemia, and diabetes.
Cerebral infarction is linked to thrombosis or embolism and results in ischemic neuronal changes such as nuclear pyknosis and eosinophilic cytoplasm within 12 hours. Microglia and monocyte infiltration occur within 2 days, followed by liquefactive necrosis leading to a fluid-filled cavity and reactive astrocytes within 1-3 weeks. Gliosis, which is scar formation, can occur after several months and the infarction may progress to hemorrhagic infarction.
Watershed infarction is linked to low blood pressure and manifests as a wedge-shaped infarction at the border of the artery's supply area, typically found between the distribution of the anterior cerebral artery (ACA) and middle cerebral artery (MCA).
Lacunar infarcts are linked to high blood pressure and blockage of small blood vessels due to blood clots, resulting in small empty spaces surrounded by scar tissue in the brain.
It varies based on the location of reduced blood flow and the degree of alternative blood supply.
Anterior Cerebral Artery (ACA): Contralateral leg weakness and sensory loss.
Middle Cerebral Artery (MCA) presents with contralateral paralysis, sensory loss, contralateral hemianopia, and aphasias.
Proximal Cerebral Artery (PCA) symptoms include contralateral sensory disruption and homonymous hemianopia, with or without macular-sparing.
Damage to the lateral striate arteries results in contralateral paralysis.
Administer thrombolytic therapy after 4.5 hours of symptom onset if no signs of hemorrhage. Use antiplatelet medication such as aspirin and dipyridamole. Modify risk factors by treating hypertension and hyperlipidemia.
A transient ischemic attack is a temporary episode of neurological symptoms resulting from reduced blood flow to the brain, which typically lasts less than 24 hours and indicates a high risk of a future stroke.
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Pathology - Hemorrhagic Stroke
Primarily caused by hypertension, other factors may include bleeding disorders, anticoagulant medication use, arteriovenous malformations, brain tumors, or amyloid angiopathy.
Pathophysiology: Chronic hypertension is linked to Charcot-Bouchard microaneurysms, typically seen in the basal ganglia. The bursting of these aneurysms may directly lead to bleeding.
Brain hemorrhage typically occurs in the basal ganglia or thalamus, with a core patch of blood surrounded by swollen brain tissue leading to edema resolution. Reactive astrocytes and macrophages then form around the injury's edge, resulting in gliosis.
Clinical Symptoms and Signs
Symptoms include altered awareness, nausea, vomiting, headache, and neurological abnormalities such as weakness on one side of the body, sensory disturbances on one side, and vision field loss.
Therapy
Treat any blood clotting disorders; closely monitor blood pressure; consider surgical decompression for significant cerebral bleeding.
Primarily caused by hypertension, other factors may include bleeding disorders, anticoagulant medication use, arteriovenous malformations, brain tumors, or amyloid angiopathy.
Pathophysiology: Chronic hypertension is linked to Charcot-Bouchard microaneurysms, typically seen in the basal ganglia. The bursting of these aneurysms may directly lead to bleeding.
Brain hemorrhage typically occurs in the basal ganglia or thalamus, with a core patch of blood surrounded by swollen brain tissue leading to edema resolution. Reactive astrocytes and macrophages then form around the injury's edge, resulting in gliosis.
Clinical Symptoms and Signs
Symptoms include altered awareness, nausea, vomiting, headache, and neurological abnormalities such as weakness on one side of the body, sensory disturbances on one side, and vision field loss.
Therapy
Treat any blood clotting disorders; closely monitor blood pressure; consider surgical decompression for significant cerebral bleeding.
