Brain Tumors
Brain tumors may be benign or malignant, primitive or metastatic. Benign tumors are most common. Malignant tumors represent about 1% of all malignancies arising. In terms of pathology, glial tumors are most common, reaching 50-60% of their percentage of the total localized primitive brain tumors. Meningiomas are found in a quarter of patients with brain tumors primitive and schwanoamele represents 10% of these tumors. The term refers to the primitive brain tumor that the tumor originates in the brain parenchyma, meninges, remains embryonic pituitary and cranial nerve roots. Metastatic brain tumor term means that the tumor of origin is somewhere other than brain tumors in the developing brain cancer cells after cantonarii at this level, cells via the blood flow coming from the tumor of origin. In the case of metastatic brain tumors, the tumor of origin can be anywhere in the body, most often being located in the lung, kidney, prostate or liver.
Brain Tumors
Metastatic brain tumors are more common than the primitive brain tumors. It is estimated that 15% of patients die annually from cancer shows symptomatic brain metastases. There are a number of pathological conditions that evolve with similar symptoms of an intracranial expansive process, but without it there. These states are known as pseudotumor cerebri, which are infections, metabolic disorders, poisoning. Topographically speaking, more than half of supratentorial brain tumors are located and the third is developing subtentorial.
Histological types of brain tumors: - Gliomas are neoformation's own nerve tissue, they developed out of supporting glial tissue and are the most common brain tumors. In most cases, gliomas are composed of a single type of cell, but several types of related, but the name is based on the tumor cell type is predominant. Gliomas grow by infiltration. Types of glial tumors Astrocytomas (are most common), ependymoma, spongioblastomul, medulloblastoma, glioblastoma multiforme. The last two types are growing rapidly in size and often recur after surgical removal. Patients with astrocytomas have a good chance of cure by surgery, but do not respond to radiotherapy. Gliomas can occur at any age, children are meeting more often medulloblastoma. With time in glioma calcifications may occur, especially if ependimoamelor and ologodendroglioamelor. - Meningiomas have a starting point of the arachnoid, are found most frequently in young adults between 20 and 45 years. Tumors are benign (except as sarcomatous). Feature is that they do not infiltrate the brain parenchyma, but it compresses, so there are chances of cure by surgical removal. These are tumors with a rich blood supply and develop in the vicinity of venous sinuses, which sometimes makes it difficult for their surgical removal. Evolving near the polar head, often found on X-ray area is the skull bone osteolysis in contact with the tumor. Types of meningiomas according to location: parasagitale meningiomas, meningiomas olfactory tubercle Bestsellers meningiomas, sphenoid wing meningiomas, meningiomas convexity, posterior cerebral fossa meningiomas. - Paraselare and pituitary adenomas is accompanied by endocrine disorders (by affecting the pituitary gland) and disorders of the visual field (hemianopsia heteronima). - Acoustic neurinomul develop the ponto-cerebellar angle, meeting at the middle-aged adults. Diagnosis should be made as soon as possible in the early stages of disease, for surgical treatment to have maximum efficiency. - Brain metastasis is made by marrow and predilection to develop in the area between the white and gray matter. The most common primary tumors of brain metastases are giving lung cancer, breast cancer (spread to the cerebellum), gastrointestinal tumors and malignant melanoma. - Other tumor types: tuberculoamele, Lueta granulomas, foreign body granulomas, vascular tumors and aneurysms, cerebral echinococcosis, cysticercosis, cerebral abscess, cerebral hematoma.
Pseudotumoral processes Brain Tumors
These pathological processes lead to intracranial hypertension, but do not fit into clinical pictures that follow. These processes are inflammatory nature: arahnoidiene cysts, Arachnoiditis the posterior fossa, Arachnoiditis optochiasmatica, inflammatory occlusion of the aqueduct of Sylvius.
Clinical Brain Tumors
Brain tumors are clinically manifested by one of the following syndromes: subacute progression of a focal neurological deficit, seizures or non-focal neurological impairment. Metastatic tumors are demonstrated by systemic symptoms as anorexia, weight loss, malaise and feeling feverish.
Focal neurological syndromes are the result of compression of white matter neurons and the effect of the tumor mass (tumor growth) and the swelling which it produces. Focal neurological syndromes are:
Frontal lobe syndrome For tumors located in the frontal lobe of the outbreak the following symptoms: psychiatric disorders, epilepsy, seizures grand mall seizures Jacksonian focused, aphasia and clips, facial nerve paresis, motor problems that become even more pronounced with more interested tumor area as the frontal lobe motor ... more about the syndrome of frontal lobe
Parietal lobe syndrome Brain Tumors
A tumor that develops in the parietal lobe gives the following clinical manifestations: - Sensitive seizures, sensitivity disorders, disorders somatognozice.
motor disorders evidenced by a slight hemiparesis, upper limb muscular atrophies controlateral (thenar and hypothenar Eminence). more about the parietal lobe syndrome
Temporal lobe syndrome If a tumor in the temporal lobe, and speech disorders are common disorders psihice.Hipertensiunea intracranial hipoestezii superficial eye disorders ... more about temporary lobe syndrome
Occipital lobe syndrome Brain Tumors
Occipital lobe tumors are rare. Visual disturbances are one of the most important signs of tumors at this level, speech disorder, if interested and parietal lobe tumor; controlaterala hemiparesis, cerebellar disorders in the form of balance disorders essentially of bulk. more about the occipital lobe syndrome
Posterior cerebral fossa syndrome Tumors that develop at this level in the cerebellum, causes serious disruptions in the normal flow of cerebrospinal fluid. Because of this, is dominated by clinical symptoms of intracranial hypertension syndrome. more about cerebral posterior fossa syndrome
Diagnostic Laboratory CT scan and MRI (magnetic resonance imaging) are imaging tests that accurately specify the topography of brain tumors. Tumors appear as formations hiperdense, replacing the space. Differential diagnosis of a cyst with fluid is easy, it appeared as a hypodense image imaging examination. It is also essential to do a biopsy to highlight the tumor histology and to guide treatment.
Treatment of Brain Tumors
It is difficult to standardize a treatment for brain tumors. In most cases this treatment involves mixed teams of surgeons, radiotherapists, chimioterapeuti and collaboration with other medical specialties. Before any surgery is performed tumor biopsy to determine histologic type of tumor. Fragment is a tumor biopsy collection to study it, and is more difficult to carry with straw as the tumor is located deep within the brain parenchyma. Histopathological examination is particularly important because it dictates treatment steps. Neurosurgical intervention aims to remove the tumor mass as possible as little damaging the brain parenchyma. The methods used are classical operators trepanarea skull, craniotomy (especially for benign tumors), craniectomia the posterior fossa. The best results are obtained by using modern means of intervention such as surgery or binocular microscope with carbon dioxide laser. In advanced stages of cancer surgery that can only do is external ventricular drainage of cerebrospinal fluid ventriculo-peritoneal or surgical treatment should be filled with the drug. It is used anticonvulsants, corticosteroids, mannitol (to reduce intracranial pressure) and type diuretic furosemide.
Prognosis of Brain Tumors
From neferiricre, the prognosis is grim in brain tumors, often not being able to remove the tumor entirely, especially if it is developed intraparenchimatos. In many cases, palliative treatment in general, improving the patient's condition, but failing to suppress the causal factor. Especially in the case of metastatic brain tumors, they are just the tip of the ice-bearg of the disease, primary tumor is usually in an advanced stage. Glucocorticoids, and anticonvulsants radiotherapy improves quality of life. Glucocorticoids in high doses have a beneficial effect on symptoms of metastases, the quality of life inbunatatindu rapidly, within hours. Anticonvulsants are used to prevent seizures or to treat any existing ones.
Showing posts with label neurological disorders. Show all posts
Showing posts with label neurological disorders. Show all posts
Friday, January 28, 2011
Ataxia disorders
Ataxia disorders
Ataxia disorders include a range of clinical manifestations including ataxia, dysarthria, intentional tremor and dismetria. Cerebellar ataxia syndrome is an injury occurred in the cerebellum, its afferent and efferent pathways, spinal cord and characterized by disorders of coordination and posture.
Patients with mental problems, ataxia gait, slurred speech, vision, inability to coordinate movements of upper limbs, tremor of the hand to grab an object incearcarea (intentional tremor).
The causes that lead to ataxia disorders - Biochemical imbalance - Metabolic - Immunological abnormalities - Intoxication with alcohol, barbiturates, paints, mercury - Primary or metastatic tumors at cerebellar - Abscesses in the subtentoriala - Bleeding or subdural hematoma in the region infratentoriala - Cerebellar infarction - Cranio-cerebral injuries with occipital head
When locating signs of neurological symptoms, impaired consciousness and occipital headache accompanied by cranial nerve paresis and weakness of the opposite side, then the most likely cause is the replacement process of space located in the cerebellar fossa.
If symptoms when it occurs slowly and insidiously cause is a metabolic or biochemical imbalance.
In case of acute onset of symptoms, intoxication with alcohol or other substances like barbiturates, diphenylhydantoin, toluene, paint, are likely to cause disturbances.
Subacute onset (in weeks) is due to the effect of toxic substances (usually alcohol) and malnutrition (in particular deficiency of vitamins B1 and B12). If the cause ataxiilor metabolic or hereditary disorders slowly and becomes permanent.
Other causes of progressive ataxia and focal neurological signs are cerebellar vascular lesions, cerebellar edema, rostral brain stem herniation, cerebellar tonsillar herniation through the occipital hole (emergency neurosurgical), lymphoma or progressive multifocal leukoencephalopathy, acute multiple sclerosis.
Cerebellar Ataxiile can be divided into two categories: acquired and inherited.
Acquired ataxia disorders
These disorders occur as a result of damage to the cerebellum and horses spinocerebeloase by trauma, infection, processes that substitute space for bleeding, tumors, or intracerebral pressure from increasing. Symptoms arising from these causes has a relatively rapid onset with cerebellar symptoms the same side as the affected portion of the cerebellum, including alteration of consciousness, paralysis of cranial nerves VI and VII. In tumors, the deficits gradually evolve, depending on the tumor growth rate. There is a special situation that develops in tumors outside the brain and cause degeneration of the cerebellum vermisului paraneoplazic through a process mediated by antibodies. In AIDS patients, they may develop an acute ataxia syndrome induced progressive multifocal leukoencephalopathy.
Other acquired causes of ataxia disorders are: - Metabolic disorders like hypothyroidism, hyponatremia, deficiency of vitamin B1 and B12 - Phenytoin poisoning, bismuth, lithium, mercury, organic solvents; - Treatment with chemotherapy; - Congenital lesions: type I Chiari malformation (the brain stem compression, congenital dilatation of the fourth ventricle due to blockage of CSF drainage in Dandy-Walker syndrome - Infectious diseases: syphilis meningeeana touch, rear syphilis - Lyme disease - infectious disease caused by the bacterium Borrelia burgdorferi, transmitted by tick bite, and besides many other things that cause facial paralysis and limb - Viral infections with polio virus, Coxsackie, echo, Epstein-Barr virus, toxoplasmosis, Legionella, and infection with prion protein responsible for Creutzfeldt-Jakob disease.
Hereditary Ataxiile
Ataxiile hereditary descendants can be transmitted either autosomal dominant or autosomal recessive, or mitochondrial mutations.
Ataxiile autosomal dominant
This category includes a variety of other conditions:
- Spinocerebeloasa ataxia type 1 - Spinocerebeloasa ataxia type 2 - Machado-Joseph disease or ataxia type 3 spinocerebeloasa
Ataxiile autosomal recessive
- Friedreich Ataxia - Ataxia-telangiectasia - Mitochondrial ataxia (cerebellar syndromes coexist with mutations in mitochondrial DNA. Some of these mutations cause ataxia.) - Xeroderma pigmentosum - Cockayne Syndrome - Marinescu-Sjogren syndrome
Ataxia disorders include a range of clinical manifestations including ataxia, dysarthria, intentional tremor and dismetria. Cerebellar ataxia syndrome is an injury occurred in the cerebellum, its afferent and efferent pathways, spinal cord and characterized by disorders of coordination and posture.
Patients with mental problems, ataxia gait, slurred speech, vision, inability to coordinate movements of upper limbs, tremor of the hand to grab an object incearcarea (intentional tremor).
The causes that lead to ataxia disorders - Biochemical imbalance - Metabolic - Immunological abnormalities - Intoxication with alcohol, barbiturates, paints, mercury - Primary or metastatic tumors at cerebellar - Abscesses in the subtentoriala - Bleeding or subdural hematoma in the region infratentoriala - Cerebellar infarction - Cranio-cerebral injuries with occipital head
When locating signs of neurological symptoms, impaired consciousness and occipital headache accompanied by cranial nerve paresis and weakness of the opposite side, then the most likely cause is the replacement process of space located in the cerebellar fossa.
If symptoms when it occurs slowly and insidiously cause is a metabolic or biochemical imbalance.
In case of acute onset of symptoms, intoxication with alcohol or other substances like barbiturates, diphenylhydantoin, toluene, paint, are likely to cause disturbances.
Subacute onset (in weeks) is due to the effect of toxic substances (usually alcohol) and malnutrition (in particular deficiency of vitamins B1 and B12). If the cause ataxiilor metabolic or hereditary disorders slowly and becomes permanent.
Other causes of progressive ataxia and focal neurological signs are cerebellar vascular lesions, cerebellar edema, rostral brain stem herniation, cerebellar tonsillar herniation through the occipital hole (emergency neurosurgical), lymphoma or progressive multifocal leukoencephalopathy, acute multiple sclerosis.
Cerebellar Ataxiile can be divided into two categories: acquired and inherited.
Acquired ataxia disorders
These disorders occur as a result of damage to the cerebellum and horses spinocerebeloase by trauma, infection, processes that substitute space for bleeding, tumors, or intracerebral pressure from increasing. Symptoms arising from these causes has a relatively rapid onset with cerebellar symptoms the same side as the affected portion of the cerebellum, including alteration of consciousness, paralysis of cranial nerves VI and VII. In tumors, the deficits gradually evolve, depending on the tumor growth rate. There is a special situation that develops in tumors outside the brain and cause degeneration of the cerebellum vermisului paraneoplazic through a process mediated by antibodies. In AIDS patients, they may develop an acute ataxia syndrome induced progressive multifocal leukoencephalopathy.
Other acquired causes of ataxia disorders are: - Metabolic disorders like hypothyroidism, hyponatremia, deficiency of vitamin B1 and B12 - Phenytoin poisoning, bismuth, lithium, mercury, organic solvents; - Treatment with chemotherapy; - Congenital lesions: type I Chiari malformation (the brain stem compression, congenital dilatation of the fourth ventricle due to blockage of CSF drainage in Dandy-Walker syndrome - Infectious diseases: syphilis meningeeana touch, rear syphilis - Lyme disease - infectious disease caused by the bacterium Borrelia burgdorferi, transmitted by tick bite, and besides many other things that cause facial paralysis and limb - Viral infections with polio virus, Coxsackie, echo, Epstein-Barr virus, toxoplasmosis, Legionella, and infection with prion protein responsible for Creutzfeldt-Jakob disease.
Hereditary Ataxiile
Ataxiile hereditary descendants can be transmitted either autosomal dominant or autosomal recessive, or mitochondrial mutations.
Ataxiile autosomal dominant
This category includes a variety of other conditions:
- Spinocerebeloasa ataxia type 1 - Spinocerebeloasa ataxia type 2 - Machado-Joseph disease or ataxia type 3 spinocerebeloasa
Ataxiile autosomal recessive
- Friedreich Ataxia - Ataxia-telangiectasia - Mitochondrial ataxia (cerebellar syndromes coexist with mutations in mitochondrial DNA. Some of these mutations cause ataxia.) - Xeroderma pigmentosum - Cockayne Syndrome - Marinescu-Sjogren syndrome
Suppurative intracranial thrombophlebitis
Suppurative intracranial thrombophlebitis
* Introduction
* Clinical
* Diagnostic Laboratory
* Treatment
Suppurative intracranial thrombophlebitis is characterized by the presence of venous thrombosis and suppurations inside the skull. This condition is the result of localized infection in sinuses or middle ear or mastoid level, oropharynx or facial skin. These infections can spread by direct or marrow and cause a suppurative thrombophlebitis within the vein or the intracranial venous sinuses. Other infectious processes can lead to intracranial vessels are trombozarea bacterial meningitis, subdural empyema or abscess epiduraln. It should be noted that this disease is quite rare and serious complication of these infectious processes, and it occurs in patients who imunotarati or congenital defects of the bones of the skull bone and allowing relatively direct communication with the interior skull skull sinuses. And rarely intracranial thrombophlebitis may occur after hematogenous dissemination of an infectious outbreak located away from the cephalic extremity, such as a chronic pulmonary infection or a kidney suppurative process.
Risk factors associated with suppurative intracranial thrombophlebitis: dehydration, pregnancy, oral contraceptive use, sickle cell anemia, polycythemia, cancer, trauma and generally states that increase blood viscosity and coagulability. Diseases that cause a high propensity for intracranial thrombophlebitis and cavernous sinus are particularly trombozarea maxillary sinusitis, frontal sinusitis, ethmoid or sphenoid, infections of the skin of the face or mouth. The most common is the maxillary sinus, it appeared as a result of an infectious process upper dental arch, following a respiratory illness, flu, or from medical maneuvers that the introduction of naso-gastric probe incompletely sterilized. Also, maxillary sinusitis and may develop after a septal deviation that obscure all or part of a nasal cavity. Because the maxillary sinus communicates through a small hole on the same side of the nasal cavity, filling it through an inflammatory process or lead to reduction or blockage of congenital sinus ventilation, with the possibility of developing germ sinus cavity. Maxillary sinus drainage hole in the nasal cavity is located higher floor away from the sinus secretions such as sinus drainage is incomplete. Because of proximity, frontal sinus and ethmoid cells quite rapidly become inflamed after maxillary sinusitis.
Etiologic agents most frequently involved in suppurative intracranial thrombosis are staphylococci, streptococci, aerobic or anaerobic, Gram-negative bacilli and anaerobic bacilli. Staphyloccusus aureus is the most common pathogen in patients with cavernous sinus thrombosis, and is found in most patients with this disorder. Less cavernous sinus thrombosis is caused by pneumococcus, streptococcus, Gram-negative bacteria or strains of Bacteroides. Usually, if after a trial sinusitis following dental infections, sinusitis germs are responsible for developing anaerobic. From here they can spread to the frontal sinus, sphenoidal and cavernous sinus to. Staphyloccusus aureus skin infections is met in the face. From the face Staphylococcus aureus can spread quite slowly, at about intracranial marrow or lymphatic, a situation more common in those cases imunotarate. Otitis media and otomastoidita can complicate the production of lateral sinus thrombosis in or sinus infections can cause upper and lower stony. Superior sagittal sinus thrombosis may occur from the release of the outbreaks of infectious germs located in the skin of the face, scalp, subdural space, epidural space. And bacterial meningitis can sometimes complicate the sagittal sinus thrombosis. At admission and initiation of empirical therapy must consider infectious outbreak that has caused intracranial thrombophlebitis, because the most likely infecting organism depends on the infectious process associated.
* Introduction
* Clinical
* Diagnostic Laboratory
* Treatment
Suppurative intracranial thrombophlebitis is characterized by the presence of venous thrombosis and suppurations inside the skull. This condition is the result of localized infection in sinuses or middle ear or mastoid level, oropharynx or facial skin. These infections can spread by direct or marrow and cause a suppurative thrombophlebitis within the vein or the intracranial venous sinuses. Other infectious processes can lead to intracranial vessels are trombozarea bacterial meningitis, subdural empyema or abscess epiduraln. It should be noted that this disease is quite rare and serious complication of these infectious processes, and it occurs in patients who imunotarati or congenital defects of the bones of the skull bone and allowing relatively direct communication with the interior skull skull sinuses. And rarely intracranial thrombophlebitis may occur after hematogenous dissemination of an infectious outbreak located away from the cephalic extremity, such as a chronic pulmonary infection or a kidney suppurative process.
Risk factors associated with suppurative intracranial thrombophlebitis: dehydration, pregnancy, oral contraceptive use, sickle cell anemia, polycythemia, cancer, trauma and generally states that increase blood viscosity and coagulability. Diseases that cause a high propensity for intracranial thrombophlebitis and cavernous sinus are particularly trombozarea maxillary sinusitis, frontal sinusitis, ethmoid or sphenoid, infections of the skin of the face or mouth. The most common is the maxillary sinus, it appeared as a result of an infectious process upper dental arch, following a respiratory illness, flu, or from medical maneuvers that the introduction of naso-gastric probe incompletely sterilized. Also, maxillary sinusitis and may develop after a septal deviation that obscure all or part of a nasal cavity. Because the maxillary sinus communicates through a small hole on the same side of the nasal cavity, filling it through an inflammatory process or lead to reduction or blockage of congenital sinus ventilation, with the possibility of developing germ sinus cavity. Maxillary sinus drainage hole in the nasal cavity is located higher floor away from the sinus secretions such as sinus drainage is incomplete. Because of proximity, frontal sinus and ethmoid cells quite rapidly become inflamed after maxillary sinusitis.
Etiologic agents most frequently involved in suppurative intracranial thrombosis are staphylococci, streptococci, aerobic or anaerobic, Gram-negative bacilli and anaerobic bacilli. Staphyloccusus aureus is the most common pathogen in patients with cavernous sinus thrombosis, and is found in most patients with this disorder. Less cavernous sinus thrombosis is caused by pneumococcus, streptococcus, Gram-negative bacteria or strains of Bacteroides. Usually, if after a trial sinusitis following dental infections, sinusitis germs are responsible for developing anaerobic. From here they can spread to the frontal sinus, sphenoidal and cavernous sinus to. Staphyloccusus aureus skin infections is met in the face. From the face Staphylococcus aureus can spread quite slowly, at about intracranial marrow or lymphatic, a situation more common in those cases imunotarate. Otitis media and otomastoidita can complicate the production of lateral sinus thrombosis in or sinus infections can cause upper and lower stony. Superior sagittal sinus thrombosis may occur from the release of the outbreaks of infectious germs located in the skin of the face, scalp, subdural space, epidural space. And bacterial meningitis can sometimes complicate the sagittal sinus thrombosis. At admission and initiation of empirical therapy must consider infectious outbreak that has caused intracranial thrombophlebitis, because the most likely infecting organism depends on the infectious process associated.
Spinal Cord Injuries
Spinal Cord Injuries
* Introduction
* Clinical
* Treatment
Most injuries are caused by spinal fractures or dislocations in the spine. Thoracic spine region is frequently affected by subsidence vertebrae fall, combined with anterior flexion of the body. Cervical spine is often affected in car accidents by hiperflexia or hyperextension of the neck. There are factors that favor the occurrence of injuries in the trauma and enhances the action of agents vulnerable. A congenitally narrow spinal canal, spondylosis disease, a hypertrophied yellow ligament or instability of the facet joints in rheumatoid arthritis predispose to severe injuries after minor trauma.
The causes of spinal cord injuries are direct and indirect. Direct causes leading to the dislocation or destruction of the vertebral body. The indirect structure does not affect the spine, but the energy is transmitted spinal injury within the spinal canal.
These injuries have the effect of producing state of concussion, compression, contusion or bone marrow section: - Medullary concussion: it is manifested by a reduction or a temporary loss of function below the area affected spinal segments. There is no structural damage but marrow. - Compression of the medulla: a syndrome characterized by neurological disorder in which bone marrow function is given by the shock of both bone marrow and the compression of the spinal cord. Bone is not structurally damaged, Aeschylus was compressed by a bone or a hematoma juxtamedular. It loses control functions controlled by spinal segments below the injury area. - Medullary contusion: in this case arising from neurological disorders, spinal structural damage by trauma, but not severed. - Section marrow: marrow in this situation is partially or completely severed. Many spinal injuries are due to secondary phenomena of the minutes and hours after the occurrence of injury. Usually, the lesions did not affect the immediate cause bone structure which has a confluence pericapilare small hemorrhages in gray matter. In about 4 hours after myocardial injury appears gray matter and white matter edema. Myocardial injury occurs at an interval of 8 hours of injury. Important to know is that necrosis and hematoma expand and occupy a segment or two above and below the main area affected. Medullary tissue is trying to recover through a process of gliosis that develops in areas of necrosis after months of injury and cause a syndrome siringomielic.
* Introduction
* Clinical
* Treatment
Most injuries are caused by spinal fractures or dislocations in the spine. Thoracic spine region is frequently affected by subsidence vertebrae fall, combined with anterior flexion of the body. Cervical spine is often affected in car accidents by hiperflexia or hyperextension of the neck. There are factors that favor the occurrence of injuries in the trauma and enhances the action of agents vulnerable. A congenitally narrow spinal canal, spondylosis disease, a hypertrophied yellow ligament or instability of the facet joints in rheumatoid arthritis predispose to severe injuries after minor trauma.
The causes of spinal cord injuries are direct and indirect. Direct causes leading to the dislocation or destruction of the vertebral body. The indirect structure does not affect the spine, but the energy is transmitted spinal injury within the spinal canal.
These injuries have the effect of producing state of concussion, compression, contusion or bone marrow section: - Medullary concussion: it is manifested by a reduction or a temporary loss of function below the area affected spinal segments. There is no structural damage but marrow. - Compression of the medulla: a syndrome characterized by neurological disorder in which bone marrow function is given by the shock of both bone marrow and the compression of the spinal cord. Bone is not structurally damaged, Aeschylus was compressed by a bone or a hematoma juxtamedular. It loses control functions controlled by spinal segments below the injury area. - Medullary contusion: in this case arising from neurological disorders, spinal structural damage by trauma, but not severed. - Section marrow: marrow in this situation is partially or completely severed. Many spinal injuries are due to secondary phenomena of the minutes and hours after the occurrence of injury. Usually, the lesions did not affect the immediate cause bone structure which has a confluence pericapilare small hemorrhages in gray matter. In about 4 hours after myocardial injury appears gray matter and white matter edema. Myocardial injury occurs at an interval of 8 hours of injury. Important to know is that necrosis and hematoma expand and occupy a segment or two above and below the main area affected. Medullary tissue is trying to recover through a process of gliosis that develops in areas of necrosis after months of injury and cause a syndrome siringomielic.
Status epilepticus
Status epilepticus
This disorder is characterized by continuous or repetitive seizures, lasting 15-30 minutes and an altered state of consciousness in interictala.
Status epilepticus is always an emergency crises often occur as a result of cardiovascular disorders, hyperthermia, metabolic imbalances that can lead to irreversible neuronal damage.
Causes The most common causes include withdrawal from anticonvulsants, metabolic imbalances, drug toxicity, infection and central nervous system tumors, cranio-cerebral trauma, refractory epilepsy.
Clinical Patients have convulsions lasting over 30 minutes, may have only mild clonic movements of the fingers or rapid eye movements. Seizures may accompany or continuous episodes of paroxysmal tachycardia, hypertension, pupillary dilatation.
Diagnosis The best method of diagnosis is conducting an EEG.
Treatment Patient came mostly in emergency and establishing an intravenous line, to solve problems and acute cardiorespiratory hyperthermia is performed quickly and neurological medical examination, laboratory blood are collected and sent to the intensive care unit where treatment is applied anticonvulsant.
Anticonvulsant treatment begins with lorazepam 0075 mg / kg iv to 2 mg / min phenytoin 20 mg / kg i.v. If seizures are not inferior to phenytoin and phenobarbital therapy continues and may even go up from sedation with barbiturates or benzodiazepines.
This disorder is characterized by continuous or repetitive seizures, lasting 15-30 minutes and an altered state of consciousness in interictala.
Status epilepticus is always an emergency crises often occur as a result of cardiovascular disorders, hyperthermia, metabolic imbalances that can lead to irreversible neuronal damage.
Causes The most common causes include withdrawal from anticonvulsants, metabolic imbalances, drug toxicity, infection and central nervous system tumors, cranio-cerebral trauma, refractory epilepsy.
Clinical Patients have convulsions lasting over 30 minutes, may have only mild clonic movements of the fingers or rapid eye movements. Seizures may accompany or continuous episodes of paroxysmal tachycardia, hypertension, pupillary dilatation.
Diagnosis The best method of diagnosis is conducting an EEG.
Treatment Patient came mostly in emergency and establishing an intravenous line, to solve problems and acute cardiorespiratory hyperthermia is performed quickly and neurological medical examination, laboratory blood are collected and sent to the intensive care unit where treatment is applied anticonvulsant.
Anticonvulsant treatment begins with lorazepam 0075 mg / kg iv to 2 mg / min phenytoin 20 mg / kg i.v. If seizures are not inferior to phenytoin and phenobarbital therapy continues and may even go up from sedation with barbiturates or benzodiazepines.
Ramsay Hunt Syndrome
Ramsay Hunt Syndrome
* Introduction
* Clinical manifestations and diagnosis
* Treatment and prognosis
Synonyms:
Hunt syndrome;
Herpes Oticus;
Ramsay Hunt syndrome is a disorder of the brain and nervous system caused by a viral infection in the brain.
This syndrome was first described in 1907 by J. Ramsay Hunt in patients with ear pain associated with skin rash and mucous membranes, which assigned the geniculate ganglion with herpes virus infection.
Etiology
Ramsay Hunt syndrome is caused by infection with varicelozosterian virus, herpes virus family. The classic symptoms of Ramsay Hunt syndrome always starts after a herpetic infection and may be associated with vertigo, hearing loss, tinnitus and facial paresis due to geniculate ganglion involvement found in the vicinity of the auditory and vestibular apparatus. Facial palsy is caused by inflammation of the facial nerve that crosses the inner ear and the media.
* Introduction
* Clinical manifestations and diagnosis
* Treatment and prognosis
Synonyms:
Hunt syndrome;
Herpes Oticus;
Ramsay Hunt syndrome is a disorder of the brain and nervous system caused by a viral infection in the brain.
This syndrome was first described in 1907 by J. Ramsay Hunt in patients with ear pain associated with skin rash and mucous membranes, which assigned the geniculate ganglion with herpes virus infection.
Etiology
Ramsay Hunt syndrome is caused by infection with varicelozosterian virus, herpes virus family. The classic symptoms of Ramsay Hunt syndrome always starts after a herpetic infection and may be associated with vertigo, hearing loss, tinnitus and facial paresis due to geniculate ganglion involvement found in the vicinity of the auditory and vestibular apparatus. Facial palsy is caused by inflammation of the facial nerve that crosses the inner ear and the media.
Marinescu-Sjogren syndrome
Marinescu-Sjogren syndrome
Marinescu-Sjogren syndrome is a rare syndrome with incompletely known pathophysiology.
It is clinically manifested as Friedreich syndrome, plus:
- cataracts
- mental retardation,
- abnormal bone
- hypogonadism and hipogonadotrop
- severe cerebellar atrophy.
Treatment is supportive including physical and occupational therapy, speech therapy and special education, therapy and hormonal treatment of hypogonadism, cataract.
Marinescu-Sjogren syndrome is a rare syndrome with incompletely known pathophysiology.
It is clinically manifested as Friedreich syndrome, plus:
- cataracts
- mental retardation,
- abnormal bone
- hypogonadism and hipogonadotrop
- severe cerebellar atrophy.
Treatment is supportive including physical and occupational therapy, speech therapy and special education, therapy and hormonal treatment of hypogonadism, cataract.
Parietal lobe syndrome
Parietal lobe syndrome A tumor that develops in the parietal lobe gives the following clinical manifestations: - Open sensory seizures, usually following the cortege of clinical manifestations. They are found in most cases of parietal lobe tumors. Specific seizure type or epileptic crisis is sensitive local sensory-motor. Such a crisis occurs in the State or the opposite cerebral hemisphere hemicorpului affected. The patient reports sensations of tingling, stinging or burning sensation in the affected limb. S and seizures have been reported with changes in body scheme, in which case the patient stated that he feels upper limb controlateral as disproportionately large or, conversely, very small, or as it perceives them as neapartinandu. - Sensitivity disorders clinic hold the key in parietal lesions. The subjective sensitivity problems and meet objectives. Subjective sensitivity problems appear as tingling or pain in the controlateral hemicorpului. They are found throughout the parietal disease. Sensitivity problems if the objective is manifested by hipoestezii parietal lesions are superficial in the deep lesions is remarkable thermal sensitivity and pain disorders. The meet, also the sensitivity epicritice disorders. In more severe cases astereognozia meets, in which the tumor affects neighboring lobes. Astereognozia manifests as an inability to recognize objects by touch, not to recognize the material they are made.
- Disorders characterized by somatognozice hemicorpului controlateral neglect, the phenomenon named hemiasomatognozie, patient hitting that mid-body objects around him. Another clinical manifestation of disorders somatognozice is unable to identify one of the fingers indicated by the examiner or may not indicate who is right or left hand. Somatognozice disorders occur more frequently in Prieta lobe lesions on non-dominant hemisphere.
Other clinical signs and symptoms that occur in the parietal lobe tumors are motor disorders evidenced by a slight hemiparesis, upper limb muscular atrophies controlateral (thenar and hypothenar Eminence). Praxice disorders occur frequently, the patient is not able to perform actions that they knew very well, considering that efectorii mechanisms are intact.
Other disorders that occur are ideomotorie apraxia, the patient can not perform simple actions, ideatorie apraxia (inability to determine the sequence of elementary acts), dressing apraxia (forget the gestures dressing patient, a phenomenon that occurs mainly in non-dominant hemisphere damage) and constructive apraxia the patient is unable to draw simple geometrical figures, even in the face model.
- Disorders characterized by somatognozice hemicorpului controlateral neglect, the phenomenon named hemiasomatognozie, patient hitting that mid-body objects around him. Another clinical manifestation of disorders somatognozice is unable to identify one of the fingers indicated by the examiner or may not indicate who is right or left hand. Somatognozice disorders occur more frequently in Prieta lobe lesions on non-dominant hemisphere.
Other clinical signs and symptoms that occur in the parietal lobe tumors are motor disorders evidenced by a slight hemiparesis, upper limb muscular atrophies controlateral (thenar and hypothenar Eminence). Praxice disorders occur frequently, the patient is not able to perform actions that they knew very well, considering that efectorii mechanisms are intact.
Other disorders that occur are ideomotorie apraxia, the patient can not perform simple actions, ideatorie apraxia (inability to determine the sequence of elementary acts), dressing apraxia (forget the gestures dressing patient, a phenomenon that occurs mainly in non-dominant hemisphere damage) and constructive apraxia the patient is unable to draw simple geometrical figures, even in the face model.
Frontal lobe syndrome
Frontal lobe syndrome For tumors located in the frontal lobe of the outbreak the following symptoms: - Psychiatric disorders: are found in most patients with tumors in the frontal lobe. Metastases and malignant gliomas are the most responsible for the occurrence of mental disorders. The frontal lobe plays a role in controlling personality, such as patients with an intracranial expansive process in the frontal lobe will show increased behavioral problems. At first interested affection. Patients become euphoric, were a permanent state of psychomotor excitation, shows an exaggerated optimism make pornographic jokes. Along with the development of tumor process, the state of euphoria is gradually replaced with a state of indifference, it alters your memory, lowers power of concentration, reduced performance at work. The frontal lobe is also a motivational center, the patient gradually loses interest in the world around them. If before the patient was very fond of and interested in the job, will get to work and even neglect their own person, will be indifferent towards the family and bystanders. Mental disorders usually accompany described above and show signs of increased intracranial pressure. These behavioral disorders can be easily confused with depression. Therefore, in such cases must be sought and any signs that could bring into question the existence of an intracranial tumor process. During the disease state meets pseudodemential syndrome, syndrome characterized by apathy, lack of will, total disregard to the surrounding world. The patient does not move, stay in one place and not only mobilizes the physiological needs. The conversation is remarkable lack of initiative, lack of interest in any subject. In advanced stages of disease when the tumor has grown much in size, meets decrease sphincter control.
- Epilepsy - this symptom occurs in more than half of patients with frontal lobe tumors. In some patients with epilepsy crisis begins adverse or generalized seizures. - Grand mall seizures are common in the tumor invades deep frontal lobe parenchyma. - Jacksonian seizures focused: they appear on the opposite half of the body affected cerebral hemisphere. These crises may be of interest strictly a particular member, superior or inferior, rarely hemicorpul all that interested. Sometimes seizures end leaves behind a transient paresis of the affected limb.
- Aphasia and clips: difficulty in speaking and writing is cursive. A feature of the aphasia and brain tumors agrafiei is that these disorders occur and evolve gradually, slowly, as the tumor increases in volume and affects more and more brain areas.
- Facial nerve paresis: paresis of VII nerve (or face) is the central type. It is accompanied by signs of pyramidal damage. Central type of facial palsy can be considered a pathognomonic sign for a growing tumor in the frontal lobe.
Other signs and symptoms that accompany brain tumors are located in the frontal lobe: motor disorders that become more pronounced with even more interested in how tumor motor area of the frontal lobe. Motor disorders usually occurs as a hemiparesis or hemiplegii affecting half the body opposite the brain hemisphere affected. In the frontal lobe tumors also meets forced grasping reflex. This reflex reaction is manifested by grabbing the last two fingers on each hand controlaterala when their daughter palm is stimulated by contact with an object. The reaction is involuntary and can not be stopped by the patient.
Cerebellar disorders are produced by damage dental Talamo-cortical pathways. Clinical manifestations of these disorders is materialized by cerebellar ataxia controlateral limb, hypotonia with reflex oscillation of opposite, opposing limbs dismetria adiadocokinezie (inability to make rapid alternative movements). Balance disorders occur relatively frequently and is manifested by gait and the static. Balance disorders arising in the context of a frontal lobe tumor called frontal ataxia Bruns. Also occur in most patients, impaired orientation in space, patients no longer recognize the house where they live, no longer recognize the street, etc..
- Epilepsy - this symptom occurs in more than half of patients with frontal lobe tumors. In some patients with epilepsy crisis begins adverse or generalized seizures. - Grand mall seizures are common in the tumor invades deep frontal lobe parenchyma. - Jacksonian seizures focused: they appear on the opposite half of the body affected cerebral hemisphere. These crises may be of interest strictly a particular member, superior or inferior, rarely hemicorpul all that interested. Sometimes seizures end leaves behind a transient paresis of the affected limb.
- Aphasia and clips: difficulty in speaking and writing is cursive. A feature of the aphasia and brain tumors agrafiei is that these disorders occur and evolve gradually, slowly, as the tumor increases in volume and affects more and more brain areas.
- Facial nerve paresis: paresis of VII nerve (or face) is the central type. It is accompanied by signs of pyramidal damage. Central type of facial palsy can be considered a pathognomonic sign for a growing tumor in the frontal lobe.
Other signs and symptoms that accompany brain tumors are located in the frontal lobe: motor disorders that become more pronounced with even more interested in how tumor motor area of the frontal lobe. Motor disorders usually occurs as a hemiparesis or hemiplegii affecting half the body opposite the brain hemisphere affected. In the frontal lobe tumors also meets forced grasping reflex. This reflex reaction is manifested by grabbing the last two fingers on each hand controlaterala when their daughter palm is stimulated by contact with an object. The reaction is involuntary and can not be stopped by the patient.
Cerebellar disorders are produced by damage dental Talamo-cortical pathways. Clinical manifestations of these disorders is materialized by cerebellar ataxia controlateral limb, hypotonia with reflex oscillation of opposite, opposing limbs dismetria adiadocokinezie (inability to make rapid alternative movements). Balance disorders occur relatively frequently and is manifested by gait and the static. Balance disorders arising in the context of a frontal lobe tumor called frontal ataxia Bruns. Also occur in most patients, impaired orientation in space, patients no longer recognize the house where they live, no longer recognize the street, etc..
Cockayne syndrome
Cockayne syndrome
Cockayne syndrome was first described in 1936 by English doctor Cockayne. It is a rare disorder associated with trisomy 20.
It is characterized by:
- mental retardation,
- optic atrophy,
- dwarfism,
- perception deafness,
- skin hypersensitivity to sunlight,
- pigmentary degeneration of the retina and
- cataracts.
You can also meet:
- deficits in cerebellar, pyramidal and extrapyramidal,
- peripheral neuropathy
- normal pressure hydrocephalus.
Patients may suffer from a facial deformity called "chicken head facies"
Cockayne syndrome was first described in 1936 by English doctor Cockayne. It is a rare disorder associated with trisomy 20.
It is characterized by:
- mental retardation,
- optic atrophy,
- dwarfism,
- perception deafness,
- skin hypersensitivity to sunlight,
- pigmentary degeneration of the retina and
- cataracts.
You can also meet:
- deficits in cerebellar, pyramidal and extrapyramidal,
- peripheral neuropathy
- normal pressure hydrocephalus.
Patients may suffer from a facial deformity called "chicken head facies"
Cranial nerve syndromes
Cranial nerve syndromes Foix Syndrome It is also called cavernous sinus syndrome. It translates clinically by edema and ptosis, cranial nerve palsy III, IV and VI. Headquarters is at the crack sphenoid lesion. Syndrome are common cause of invasive tumors and aneurysms of the sphenoid bone.
Tolosa-Hunt syndrome Foix- Clinically resemble cavernous sinus syndrome. Are affected cranial nerves III, IV, the first branch of the trigeminal nerve and the nerve VI. The seat of the lesion is at the side wall of the cavernous sinus. Common causes are aneurysms and cavernous sinus thrombosis, invasive tumors of the cavernous sinus and Turkish saddle, benign granulomas.
Jacod syndrome It is clinically manifested by unilateral blindness and hemiplegia ophthalmoplegic with facial or trigeminal neuralgia. Are affected cranial nerves II, III, IV, V and VI. Headquarters retrosfenoidal lesion is in the space. Common causes are tumors of middle cranial fossa capacitive, the temporal fossa, intracondilian that compress the nerves. This syndrome is also known as syndrome carefurului petrosfenoid.
Gradenigo syndrome Involves pairs of cranial nerves affecting the V and VI. Headquarters is located at the tip lesion bone rock. The etiology of this syndrome is a localized osteitis stones or a tumor in the internal auditory canal.
Collet-Sicard syndrome It is a syndrome caused by damage to the pairs of cranial nerves IX, X, XI and XII. Hemiplegia is characterized by language and by the same party events Vernet syndrome - hemianestezia hemiparalizia and soft palate, pharynx and larynx, unilateral paralysis of the trapezius and sternocleidomastoid muscle. Headquarters laterocondilian lesion is in the rear space. The cause is the parotid gland tumors, the carotid glomusului, tumors of the lymph nodes and metastatic tumors.
Villaret syndrome It is a group of disorders caused by unilateral and simultaneous paralysis of the last four pairs of cranial nerves IX, X, XI and XII and the sympathetic nervous thread. Clinic is characterized by hemiparalizie gloso-palato-pharyngo-larynx with hemianestezie, swallowing and phonation disorders and symptoms characteristic of Horner syndrome - miosis, ptosis and decreased facial sudoratiei same side. Headquarters retroparotidian lesions is the posterior space. The most frequent causes of the syndrome are tumors of the parotid gland, the carotid glomusului, the lymph nodes, tumor metastasis and adena TB.
Tolosa-Hunt syndrome Foix- Clinically resemble cavernous sinus syndrome. Are affected cranial nerves III, IV, the first branch of the trigeminal nerve and the nerve VI. The seat of the lesion is at the side wall of the cavernous sinus. Common causes are aneurysms and cavernous sinus thrombosis, invasive tumors of the cavernous sinus and Turkish saddle, benign granulomas.
Jacod syndrome It is clinically manifested by unilateral blindness and hemiplegia ophthalmoplegic with facial or trigeminal neuralgia. Are affected cranial nerves II, III, IV, V and VI. Headquarters retrosfenoidal lesion is in the space. Common causes are tumors of middle cranial fossa capacitive, the temporal fossa, intracondilian that compress the nerves. This syndrome is also known as syndrome carefurului petrosfenoid.
Gradenigo syndrome Involves pairs of cranial nerves affecting the V and VI. Headquarters is located at the tip lesion bone rock. The etiology of this syndrome is a localized osteitis stones or a tumor in the internal auditory canal.
Collet-Sicard syndrome It is a syndrome caused by damage to the pairs of cranial nerves IX, X, XI and XII. Hemiplegia is characterized by language and by the same party events Vernet syndrome - hemianestezia hemiparalizia and soft palate, pharynx and larynx, unilateral paralysis of the trapezius and sternocleidomastoid muscle. Headquarters laterocondilian lesion is in the rear space. The cause is the parotid gland tumors, the carotid glomusului, tumors of the lymph nodes and metastatic tumors.
Villaret syndrome It is a group of disorders caused by unilateral and simultaneous paralysis of the last four pairs of cranial nerves IX, X, XI and XII and the sympathetic nervous thread. Clinic is characterized by hemiparalizie gloso-palato-pharyngo-larynx with hemianestezie, swallowing and phonation disorders and symptoms characteristic of Horner syndrome - miosis, ptosis and decreased facial sudoratiei same side. Headquarters retroparotidian lesions is the posterior space. The most frequent causes of the syndrome are tumors of the parotid gland, the carotid glomusului, the lymph nodes, tumor metastasis and adena TB.
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