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48 Cards in this Set
- Front
- Back
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(GUNNER) - Spina bifida
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– failure of posterior vertebral arches to close. Several forms which include:
1) Meningocele – herniated membranes consisting of only meninges 2) Meningomyelocele – herniated meninges and spinal cord 3) Spinal bifida occulta – vertebral \arches do not form in lumbar area but spinal cord is normal. No symptoms, may have a lumbar dimple, lipoma, or tuft of hair on exam. |
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(GUNNER)- Arnold-Chiari malformation
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Downward displacement of cerebellar tonsils and medulla through the foramen magnum
Results in obstruction of CSF (cerebrospinal fluid) outflow tract and causes hydrocephalus. May present with headaches, visual changes, seizures or confusion. Increased incidence of coexisting thoracolumbar meningomyelocele or syringomyelia (most common at C8-T1) |
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(GUNNER)- Fetal alcohol syndrome:
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most common cause of mental retardation (affecting 1 - 4.8 per 1000 children born in the US) — versus:
- Down syndrome: most common genetic cause of mental retardation - Fragile X syndrome: most common inherited cause of mental retardation Mental retardation due to CNS (central nervous system) damage: - prenatal alcohol exposure (especially during the first trimester) may disrupt crucial developmental pathways, including the retinoic acid and Hedgehog pathways Growth retardation → - small body size - microcephaly - midface hypoplasia Midface abnormalities: 1) short palpebral fissures 2) epicanthal folds 3) long philtrum 4) thin upper lip Heart defects: - VSD (ventricular septal defect) - ASD (atrial septal defect) |
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(GUNNER) - TORCHeS infections:
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Toxoplasma
Rubella CMV Herpes simplex, HIV Syphilis - Associated symptoms include microcephaly, jaundice or hepatosplenomegaly. |
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(GUNNER)- Neural tube defects
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Associated with increased alpha fetoprotein in amniotic fluid
Associated with maternal folic acid deficiency |
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(GUNNER)- Fragile X Syndrome
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200 or more CGG repeats on the X chromosome.
- X-linked dominant inheritance -Associated with large testes (macro-orchidism), large jaw, large ears |
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(GUNNER) Myotonic Dystrophy:
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> 50 CTG repeats of the gene for myotonic dystrophy protein kinase on chromosome 19
-Autosomal dominant inheritance |
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(GUNNER) - Loss of the paternal alleles → Prader-Willi syndrome
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The involved genes are still being investigated
Sx: obesity, mental retardation, neonatal hypotonia (hallmark feature) |
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(GUNNER)- NF (neurofibromatosis) type 1: diagnosis is made if
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diagnosis is made if a patient has ≥2 of the "cannot fail to be first" criteria — "CA NN OT FAI L 2 B 1st":
CA — ≥6 CAfé au lait (coffee-colored) macules (≥5mm in kids; ≥15mm in adults) NN — ≥2 Neurofibromas (flesh-colored skin nodules secondary to Schwann cell proliferation) or ≥1 plexiform neurofibroma OT — OpTic gliomas FAI — Freckling: Axillary or Inguinal L 2 — ≥2 Lisch nodules (pigmented iris hamartomas) B — Bone abnormality, for example: - kyphoscoliosis - tibial dysplasia → bowing of tibia - sphenoid dysplasia 1st — ≥1 1st degree relative with neurofibromatosis type 1 |
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(GUNNER)-
Phakomatoses (Neurocutaneous Syndromes) |
Phakomatosis incidence: NF (neurofibromatosis) > TS (tuberous sclerosis) > SWS (Sturge-Weber syndrome)
Inheritance: - NF: autosomal dominant with variable expression - TS: autosomal dominant - SWS: sometimes due to somatic mosaicism, other times due to sporadic mutation NF type 1: associated with mutation of a tumor suppressor gene called neurofibromin (which inhibits the p21 ras oncoprotein) on chromosome 17 ∴ overactivity of ras may cause some of the manifestations of NF type 1 NF type 2: associated with mutation in a tumor suppressor gene called merlin (a critical regulator of contact-dependent inhibition of proliferation) on chromosome 22 TS: associated with mutations of two genes: - TSC1 gene (chromosome 9) — codes for a protein called hamartin, which regulates the cell-cycle, neuronal synapse formation and axon development - TSC2 gene (chromosome 16) — codes for a protein called tuberin, which has GTPase-activating activity and regulates protein translation, growth and cell proliferation - hamartin and tuberin form heterodime |
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(GUNNER) - Malignancies associated with NF type 1 include:
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pheochromocytoma
Wilm's tumor juvenile CML (chronic myelogenous leukemia) Note: pheochromocytoma and Wilm's tumor are both associated with hypertension |
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(GUNNER) - NF (neurofibromatosis) type 2: diagnosis is made if
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diagnosis is made if a patient has bilateral acoustic neuromas (benign schwannomas of vestibular division of CN8), which may present as sensorineural hearing loss, tinnitus, and vestibular disorientation.
Besides bilateral acoustic neuromas, other findings associated with neurofibromatosis type 2 include: - juvenile cataracts in ~80% of patients - schwannomas — e.g., unilateral acoustic neuromas, spinal schwannomas - meningiomas - gliomas Like NF type 1, patients with NF type 2 may have: - café au lait (coffee-colored) macules - cutaneous neurofibromas |
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(GUNNER) - TS (tuberous sclerosis): use the mnemonic "AASS RRRASH":
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Ash Leaf Spots: Hypopigmented spots often found on the skin of TS patients
Angiofibromas (adenoma sebaceum) of the face: reddish brown papules on the nose and cheeks in a butterfly distribution Shagreen patches: rough papules with orange-peel consistency usually on the trunk - best identified with a Wood's lamp (UV-A light) Seizures (infantile spasms) Retardation (mental) Retinal lesions: - mulberry tumors - phakomas: round flat gray lesions located peripherally in the retina Rhabdomyomas in the heart → may cause CHF (congestive heart failure) - a cardiac rhabdomyoma in a young child is highly suspicious (nearly 100% specific) for tuberous sclerosis Angiomyolipomas of the kidney: hamartomatous lesions Subependymal astrocyte proliferation in the brain: hamartomatous lesions that look like "candlestick dripping" in cerebral ventricles - multinucleated atypical astrocytes may also form tubers (small white nodules) in cerebral cortex and periventricular locations Hamartomas |
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(GUNNER) - Sturge-Weber Syndrome (encephalotrigeminal angiomatosis):
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rare congenital syndrome characterized by:
1) Neurologic deterioration 2) Facial port-wine stain nevus flammeus "birthmark" in the trigeminal nerve distribution 3) Leptomeningeal hemangiomas 4) Buphthalmos (markedly enlarged eye) Children develop progressive neurologic deterioration: - Seizures - Mental retardation - Hemiparesis - Hemisensory deficit Port-wine stain nevus flammeus "birthmark": - Macular vascular lesion (congenital unilateral capillary or cavernous hemangioma) on the face in the dermatomal distribution of cranial nerve V — usually the V1 or V2 dermatomal distribution - Does not blanch with pressure Some patients have an ipsilateral arteriovenous malformation of pia mater vessels (ipsilateral leptomeningeal angioma) overlying occipital and parietal lobes Skull X-ray of patients after 2 years of age: - Gyriform "tramline" intracranial calcifications Children often suffer from visual disturbances (eg, hemianopia) and often present with buphthalmos (markedly enlarged eye): - Congenital glaucoma → retained aqueous humor → buphthalmos |
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(GUNNER) - Vertigo:
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illusion of rotary movement caused by an acute asymmetry of neural impulses between left and right vestibular systems
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(GUNNER)- Peripheral vertigo:
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all etiologies involve the inner ear (most common: benign paroxysmal positional vertigo, acute vestibular neuronitis, and Ménière’s disease)
- Clues to peripheral vertigo: tinnitus, hearing loss, prominent nausea and vomiting - Benign paroxysmal positional vertigo (BPPV): brief periods of vertigo which occur with change in position due to freely moving crystals of calcium carbonate within one of the semicircular canals -Ménière’s disease: intermittent increase in endolymphatic volume of the inner ear causing episodic vertigo with nausea, vomiting, progressive hearing loss, and a sensation of fullness in the ear -Positional testing: delayed horizontal nystagmus, inhibited by fixation of eyes onto object, and does not change direction with gaze to either side |
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(GUNNER) - Central vertigo:
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results from cerebellar or brainstem lesion and usually associated with cranial nerve signs (e.g. diplopia, dysarthria, dysphagia), weakness, ataxia, or other changes that indicate a central process
Clues to central vertigo: severe inability to stand still or walk Positional testing: immediate vertical, horizontal, or torsional (rotary) nystagmus, not inhibited by fixation of eyes onto object, and can change direction with gaze towards fast phase of nystagmus |
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(GUNNER) - Strokes of the vertebrobasilar system:
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strokes in this region spare higher functioning, unlike cerebral artery strokes, but affect structures like the cerebellum and brainstem, resulting in ipsilateral motor symptoms and cranial nerve deficits.
Locked-in syndrome: infarcts of the pons. It severs corticobulbar, corticospinal, and corticopontine tracts, resulting in complete paralysis except for vertical eye movements, the nerves for which exit the brainstem above the level of the lesion. Lateral medullary syndrome (Wallenberg's syndrome): infarcts of the vertebral artery or PICA, and causes ipsilateral ataxia, facial pain sense loss, temperature sense loss, Horner's syndrome, and decreased taste, with contralateral decreased pain and temperature sense in the body, and hoarseness, dysphagia, vertigo, nystagmus, and nausea. Key diagnostic feature: involvement of autonomic nervous system (Horner's snydrome and nausea) and cranial nerves (vertigo, nystagmus, dysphagia, hoarseness). Medial medullary syndrome: infarcts of the paramedian branches of vertebral and anterior spinal arteries. It results in contralateral arm or leg weakness, contralateral decreased position and vibration sense, and ipsilateral tongue weakness. Key diagnostic feature: involvement of hypoglossal nucleus (tongue weakness) without other cranial nerve deficits. |
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(GUNNER) - Lacunar infarcts are often the result of small vessel disease caused by chronic hypertension.
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Pure sensory strokes (thalamic lacune): infarcts of ventral posterior lateral nucleus of the thalamus result in sensory loss to the contralateral body and infarcts of ventral posterior medial nucleus result in sensory loss of the contralateral face.
Pure motor strokes (hemiparesis with dysarthria and ataxic hemiparesis): infarcts of the posterior limb of the internal capsule and ventral pons. Sensorimotor strokes (having both symptoms of pure sensory strokes and pure motor hemiparesis): infarcts of the internal capsule + regions of the thalamus. |
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(GUNNER) - Occlusions of one of the three major cerebral arteries produce a specific pattern of symptoms.
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Anterior cerebral artery (ACA) infarcts: upper motor-neuron weakness and cortical-type sensory loss in the contralateral leg.
Posterior cerebral artery (PCA) infarcts: contralateral homonymous hemianopia. PCA infarcts can also affect the thalamus or posterior limbs of the internal capsule, resulting in contralateral hemiparesis or sensory loss. Middle cerebral artery (MCA) infarcts: aphasia (Broca's or motor aphasia), hemineglect, hemianopia, and face-arm sensorimotor loss. There is sometimes gaze preference toward the same side as the lesion. MCA infarcts are common. |
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(GUNNER)- Hemorrhagic strokes (intracerebral hemorrhages): rupture of cerebral blood vessel.
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Hemorrhagic strokes are typically caused by embolisms rather than thromboses.
Recall that embolism → ischemic stroke → converts to hemorrhagic stroke Most common causes: hypertension, amyloid angiopathy, and vascular malformations. Ischemic strokes can also transform into hemorrhagic strokes, due to disruption of the blood brain barrier and leakage of red blood cells into ischemic tissue, or leakage of capillaries during reperfusion of infarcted tissue. |
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(GUNNER) - Ischemic strokes: inadequate blood supply to a region of the brain, due to thrombosis or embolism
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Ischemic strokes can be caused by embolisms or thromboses. Most strokes are ischemic, rather than hemorrhagic.
Tx: anticoagulants. In the emergency room setting, recombinant tissue plasminogen activator (rtPA or tPA) is the treatment of choice. Administration should be within 3 to 4.5 hours of onset of symptoms. Transient Ischemic Attacks (TIAs): occlusion of blood flow for only a short period of time. Usually caused by fragments of atherosclerotic plaques that embolize (often from carotids). By definition, the deficits of TIAs last less than 24 hours, but TIAs can precede strokes causing permanent deficits. |
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(GUNNER) - Cerebrovascular infarctions: vascular occlusion secondary to thombosis or embolism. Can be long lasting and disabling, or transient.
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Two types of stroke: ischemic and hemorrhagic.
Two regions of an infarct: Core: receives blood only from the occluded artery. Most at risk for lasting damage. Penumbra: borders the core, perfused by other arteries, greater chance of surviving the infarction due to collateral blood flow. Watershed infarcts: occlusion of multiple arteries results in "watershed infarcts." Areas supplied by multiple occluded arteries are at greater risk of permanent injury. Infarcted brain tissue is cleared by macrophages and undergoes liquefactive or coagulative necrosis. CT is used to differentiate ischemic from hemorrhagic. First step in diagnosis of suspected stroke. Non-contrast CT is best for identifying hemorrhagic strokes. Ischemic strokes are not usually visible on CT scans. MRI is required to diagnose ischemic strokes. |
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(GUNNER) - Tuberculoid:leprosy
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Tuberculoid: host has vigorous cellular immune response to infection (reactive skin tests) because it predominately activates Th1 cells → activates cell mediated response → very effective defense against intracellular bacteria
- Disease is self-limited. Affects skin and peripheral nerves. Rarely fatal if treated. Most common morbidity: ulnar nerve injury, esp. in tuberculoid form |
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(GUNNER) - Spina bifida
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– failure of posterior vertebral arches to close. Several forms which include:
1) Meningocele – herniated membranes consisting of only meninges 2) Meningomyelocele – herniated meninges and spinal cord 3) Spinal bifida occulta – vertebral \arches do not form in lumbar area but spinal cord is normal. No symptoms, may have a lumbar dimple, lipoma, or tuft of hair on exam. |
|
|
(GUNNER)- Arnold-Chiari malformation
|
Downward displacement of cerebellar tonsils and medulla through the foramen magnum
Results in obstruction of CSF (cerebrospinal fluid) outflow tract and causes hydrocephalus. May present with headaches, visual changes, seizures or confusion. Increased incidence of coexisting thoracolumbar meningomyelocele or syringomyelia (most common at C8-T1) |
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|
(GUNNER)- Fetal alcohol syndrome:
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most common cause of mental retardation (affecting 1 - 4.8 per 1000 children born in the US) — versus:
- Down syndrome: most common genetic cause of mental retardation - Fragile X syndrome: most common inherited cause of mental retardation Mental retardation due to CNS (central nervous system) damage: - prenatal alcohol exposure (especially during the first trimester) may disrupt crucial developmental pathways, including the retinoic acid and Hedgehog pathways Growth retardation → - small body size - microcephaly - midface hypoplasia Midface abnormalities: 1) short palpebral fissures 2) epicanthal folds 3) long philtrum 4) thin upper lip Heart defects: - VSD (ventricular septal defect) - ASD (atrial septal defect) |
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(GUNNER) - TORCHeS infections:
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Toxoplasma
Rubella CMV Herpes simplex, HIV Syphilis - Associated symptoms include microcephaly, jaundice or hepatosplenomegaly. |
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|
(GUNNER)- Neural tube defects
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Associated with increased alpha fetoprotein in amniotic fluid
Associated with maternal folic acid deficiency |
|
|
(GUNNER)- Fragile X Syndrome
|
200 or more CGG repeats on the X chromosome.
- X-linked dominant inheritance -Associated with large testes (macro-orchidism), large jaw, large ears |
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|
(GUNNER) Myotonic Dystrophy:
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> 50 CTG repeats of the gene for myotonic dystrophy protein kinase on chromosome 19
-Autosomal dominant inheritance |
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(GUNNER) - Loss of the paternal alleles → Prader-Willi syndrome
|
The involved genes are still being investigated
Sx: obesity, mental retardation, neonatal hypotonia (hallmark feature) |
|
|
(GUNNER)- NF (neurofibromatosis) type 1: diagnosis is made if
|
diagnosis is made if a patient has ≥2 of the "cannot fail to be first" criteria — "CA NN OT FAI L 2 B 1st":
CA — ≥6 CAfé au lait (coffee-colored) macules (≥5mm in kids; ≥15mm in adults) NN — ≥2 Neurofibromas (flesh-colored skin nodules secondary to Schwann cell proliferation) or ≥1 plexiform neurofibroma OT — OpTic gliomas FAI — Freckling: Axillary or Inguinal L 2 — ≥2 Lisch nodules (pigmented iris hamartomas) B — Bone abnormality, for example: - kyphoscoliosis - tibial dysplasia → bowing of tibia - sphenoid dysplasia 1st — ≥1 1st degree relative with neurofibromatosis type 1 |
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(GUNNER)-
Phakomatoses (Neurocutaneous Syndromes) |
Phakomatosis incidence: NF (neurofibromatosis) > TS (tuberous sclerosis) > SWS (Sturge-Weber syndrome)
Inheritance: - NF: autosomal dominant with variable expression - TS: autosomal dominant - SWS: sometimes due to somatic mosaicism, other times due to sporadic mutation NF type 1: associated with mutation of a tumor suppressor gene called neurofibromin (which inhibits the p21 ras oncoprotein) on chromosome 17 ∴ overactivity of ras may cause some of the manifestations of NF type 1 NF type 2: associated with mutation in a tumor suppressor gene called merlin (a critical regulator of contact-dependent inhibition of proliferation) on chromosome 22 TS: associated with mutations of two genes: - TSC1 gene (chromosome 9) — codes for a protein called hamartin, which regulates the cell-cycle, neuronal synapse formation and axon development - TSC2 gene (chromosome 16) — codes for a protein called tuberin, which has GTPase-activating activity and regulates protein translation, growth and cell proliferation - hamartin and tuberin form heterodime |
|
|
(GUNNER) - Malignancies associated with NF type 1 include:
|
pheochromocytoma
Wilm's tumor juvenile CML (chronic myelogenous leukemia) Note: pheochromocytoma and Wilm's tumor are both associated with hypertension |
|
|
(GUNNER) - NF (neurofibromatosis) type 2: diagnosis is made if
|
diagnosis is made if a patient has bilateral acoustic neuromas (benign schwannomas of vestibular division of CN8), which may present as sensorineural hearing loss, tinnitus, and vestibular disorientation.
Besides bilateral acoustic neuromas, other findings associated with neurofibromatosis type 2 include: - juvenile cataracts in ~80% of patients - schwannomas — e.g., unilateral acoustic neuromas, spinal schwannomas - meningiomas - gliomas Like NF type 1, patients with NF type 2 may have: - café au lait (coffee-colored) macules - cutaneous neurofibromas |
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|
(GUNNER) - TS (tuberous sclerosis): use the mnemonic "AASS RRRASH":
|
Ash Leaf Spots: Hypopigmented spots often found on the skin of TS patients
Angiofibromas (adenoma sebaceum) of the face: reddish brown papules on the nose and cheeks in a butterfly distribution Shagreen patches: rough papules with orange-peel consistency usually on the trunk - best identified with a Wood's lamp (UV-A light) Seizures (infantile spasms) Retardation (mental) Retinal lesions: - mulberry tumors - phakomas: round flat gray lesions located peripherally in the retina Rhabdomyomas in the heart → may cause CHF (congestive heart failure) - a cardiac rhabdomyoma in a young child is highly suspicious (nearly 100% specific) for tuberous sclerosis Angiomyolipomas of the kidney: hamartomatous lesions Subependymal astrocyte proliferation in the brain: hamartomatous lesions that look like "candlestick dripping" in cerebral ventricles - multinucleated atypical astrocytes may also form tubers (small white nodules) in cerebral cortex and periventricular locations Hamartomas |
|
|
(GUNNER) - Sturge-Weber Syndrome (encephalotrigeminal angiomatosis):
|
rare congenital syndrome characterized by:
1) Neurologic deterioration 2) Facial port-wine stain nevus flammeus "birthmark" in the trigeminal nerve distribution 3) Leptomeningeal hemangiomas 4) Buphthalmos (markedly enlarged eye) Children develop progressive neurologic deterioration: - Seizures - Mental retardation - Hemiparesis - Hemisensory deficit Port-wine stain nevus flammeus "birthmark": - Macular vascular lesion (congenital unilateral capillary or cavernous hemangioma) on the face in the dermatomal distribution of cranial nerve V — usually the V1 or V2 dermatomal distribution - Does not blanch with pressure Some patients have an ipsilateral arteriovenous malformation of pia mater vessels (ipsilateral leptomeningeal angioma) overlying occipital and parietal lobes Skull X-ray of patients after 2 years of age: - Gyriform "tramline" intracranial calcifications Children often suffer from visual disturbances (eg, hemianopia) and often present with buphthalmos (markedly enlarged eye): - Congenital glaucoma → retained aqueous humor → buphthalmos |
|
|
(GUNNER) - Vertigo:
|
illusion of rotary movement caused by an acute asymmetry of neural impulses between left and right vestibular systems
|
|
|
(GUNNER)- Peripheral vertigo:
|
all etiologies involve the inner ear (most common: benign paroxysmal positional vertigo, acute vestibular neuronitis, and Ménière’s disease)
- Clues to peripheral vertigo: tinnitus, hearing loss, prominent nausea and vomiting - Benign paroxysmal positional vertigo (BPPV): brief periods of vertigo which occur with change in position due to freely moving crystals of calcium carbonate within one of the semicircular canals -Ménière’s disease: intermittent increase in endolymphatic volume of the inner ear causing episodic vertigo with nausea, vomiting, progressive hearing loss, and a sensation of fullness in the ear -Positional testing: delayed horizontal nystagmus, inhibited by fixation of eyes onto object, and does not change direction with gaze to either side |
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(GUNNER) - Central vertigo:
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results from cerebellar or brainstem lesion and usually associated with cranial nerve signs (e.g. diplopia, dysarthria, dysphagia), weakness, ataxia, or other changes that indicate a central process
Clues to central vertigo: severe inability to stand still or walk Positional testing: immediate vertical, horizontal, or torsional (rotary) nystagmus, not inhibited by fixation of eyes onto object, and can change direction with gaze towards fast phase of nystagmus |
|
|
(GUNNER) - Strokes of the vertebrobasilar system:
|
strokes in this region spare higher functioning, unlike cerebral artery strokes, but affect structures like the cerebellum and brainstem, resulting in ipsilateral motor symptoms and cranial nerve deficits.
Locked-in syndrome: infarcts of the pons. It severs corticobulbar, corticospinal, and corticopontine tracts, resulting in complete paralysis except for vertical eye movements, the nerves for which exit the brainstem above the level of the lesion. Lateral medullary syndrome (Wallenberg's syndrome): infarcts of the vertebral artery or PICA, and causes ipsilateral ataxia, facial pain sense loss, temperature sense loss, Horner's syndrome, and decreased taste, with contralateral decreased pain and temperature sense in the body, and hoarseness, dysphagia, vertigo, nystagmus, and nausea. Key diagnostic feature: involvement of autonomic nervous system (Horner's snydrome and nausea) and cranial nerves (vertigo, nystagmus, dysphagia, hoarseness). Medial medullary syndrome: infarcts of the paramedian branches of vertebral and anterior spinal arteries. It results in contralateral arm or leg weakness, contralateral decreased position and vibration sense, and ipsilateral tongue weakness. Key diagnostic feature: involvement of hypoglossal nucleus (tongue weakness) without other cranial nerve deficits. |
|
|
(GUNNER) - Lacunar infarcts are often the result of small vessel disease caused by chronic hypertension.
|
Pure sensory strokes (thalamic lacune): infarcts of ventral posterior lateral nucleus of the thalamus result in sensory loss to the contralateral body and infarcts of ventral posterior medial nucleus result in sensory loss of the contralateral face.
Pure motor strokes (hemiparesis with dysarthria and ataxic hemiparesis): infarcts of the posterior limb of the internal capsule and ventral pons. Sensorimotor strokes (having both symptoms of pure sensory strokes and pure motor hemiparesis): infarcts of the internal capsule + regions of the thalamus. |
|
|
(GUNNER) - Occlusions of one of the three major cerebral arteries produce a specific pattern of symptoms.
|
Anterior cerebral artery (ACA) infarcts: upper motor-neuron weakness and cortical-type sensory loss in the contralateral leg.
Posterior cerebral artery (PCA) infarcts: contralateral homonymous hemianopia. PCA infarcts can also affect the thalamus or posterior limbs of the internal capsule, resulting in contralateral hemiparesis or sensory loss. Middle cerebral artery (MCA) infarcts: aphasia (Broca's or motor aphasia), hemineglect, hemianopia, and face-arm sensorimotor loss. There is sometimes gaze preference toward the same side as the lesion. MCA infarcts are common. |
|
|
(GUNNER)- Hemorrhagic strokes (intracerebral hemorrhages): rupture of cerebral blood vessel.
|
Hemorrhagic strokes are typically caused by embolisms rather than thromboses.
Recall that embolism → ischemic stroke → converts to hemorrhagic stroke Most common causes: hypertension, amyloid angiopathy, and vascular malformations. Ischemic strokes can also transform into hemorrhagic strokes, due to disruption of the blood brain barrier and leakage of red blood cells into ischemic tissue, or leakage of capillaries during reperfusion of infarcted tissue. |
|
|
(GUNNER) - Ischemic strokes: inadequate blood supply to a region of the brain, due to thrombosis or embolism
|
Ischemic strokes can be caused by embolisms or thromboses. Most strokes are ischemic, rather than hemorrhagic.
Tx: anticoagulants. In the emergency room setting, recombinant tissue plasminogen activator (rtPA or tPA) is the treatment of choice. Administration should be within 3 to 4.5 hours of onset of symptoms. Transient Ischemic Attacks (TIAs): occlusion of blood flow for only a short period of time. Usually caused by fragments of atherosclerotic plaques that embolize (often from carotids). By definition, the deficits of TIAs last less than 24 hours, but TIAs can precede strokes causing permanent deficits. |
|
|
(GUNNER) - Cerebrovascular infarctions: vascular occlusion secondary to thombosis or embolism. Can be long lasting and disabling, or transient.
|
Two types of stroke: ischemic and hemorrhagic.
Two regions of an infarct: Core: receives blood only from the occluded artery. Most at risk for lasting damage. Penumbra: borders the core, perfused by other arteries, greater chance of surviving the infarction due to collateral blood flow. Watershed infarcts: occlusion of multiple arteries results in "watershed infarcts." Areas supplied by multiple occluded arteries are at greater risk of permanent injury. Infarcted brain tissue is cleared by macrophages and undergoes liquefactive or coagulative necrosis. CT is used to differentiate ischemic from hemorrhagic. First step in diagnosis of suspected stroke. Non-contrast CT is best for identifying hemorrhagic strokes. Ischemic strokes are not usually visible on CT scans. MRI is required to diagnose ischemic strokes. |
|
|
(GUNNER) - Tuberculoid:leprosy
|
Tuberculoid: host has vigorous cellular immune response to infection (reactive skin tests) because it predominately activates Th1 cells → activates cell mediated response → very effective defense against intracellular bacteria
- Disease is self-limited. Affects skin and peripheral nerves. Rarely fatal if treated. Most common morbidity: ulnar nerve injury, esp. in tuberculoid form |
