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• Pilocytic (low-grade) astrocytoma - Most common 1° brain tumor in childhood.- Usually well circumscribed.- In children, most often found in posterior fossa (eg, cerebellum).- May be supratentorial.- Benign, good prognosis. - Glial cell origin, GFAP ⊕.- Rosenthal fibres – eosinophilic, corkscrew fibers.- Cystic + solid (gross).- Spindle cells with hair-like glial processes that are associated with microcysts
• Medulloblastoma - Most common malignant brain tumor in childhood. - Commonly involves cerebellum.- Can compress 4th ventricle, causing noncommunicating hydrocephalus → headaches, papilledema.- Can send "drop metastases" to spinal cord. - A form of primitive neuroectodermal tumor (PNET).- Homer-Wright rosettes, small, round blue cells.- Abundant mitoses.
• Ependymoma - Most commonly found in 4th ventricle.- Can cause hydrocephalus.- Poor prognosis. - Ependymal cell origin.- Characteristic perivascular pseudorosettes.- Rod-shaped blepharoplasts (basal ciliary bodies) found near the nucleus.
• Craniopharyngioma - Most common childhood supratentorial tumor.- May be confused with pituitary adenoma (both can cause bitemporal hemianopia). - Derived from remnants of Rathke pouch (ectoderm).- Calcification is common.- Cholesterol crystals found in "motor oil"-like fluid within tumor.
• Pinealoma Tumor of pineal gland. - Can cause Parinaud syndrome: compression of tectum → vertical gaze palsy, bilateral eyelid retraction (eg, Collier sign, sclera visible above the superior corneal limbus), light-near dissociation (eg, pupils that react to accomodation but not to light)- Obstructive hydrocephalus: compression of cerebral aqueduct with papilledema, headache, vomiting- Precocious puberty in males (β-hCG production) - Histologically similar to germ cell tumors (eg, testicular seminoma).
• Glioblastoma multiforme (grade IV astrocytoma) Common, highly malignant 1° brain tumor with ~1-year median survival.- Found in cerebral hemispheres.- Can cross corpus callosum ("butterfly glioma"). - "Pseudopalisading" pleomorphic tumor cells border central areas of necrosis, hemorrhage, and/or microvascular proliferation.- Astrocyte origin, GFAP ⊕.
• Oligodendroglioma Relatively rare, slow growing.- Most often in frontal lobes.- "Chicken-wire" capillary pattern. - Oligodendrocytes = "fried egg" cells – round nuclei with clear cytoplasm.- Often calcified.
• Meningioma Common, typically benign brain tumor.- Females > males.- Most often occurs near surfaces of brain and parasagittal region.- Extra-axial (external to brain parenchyma) and may have a dural attachment ("tail"). - Often asymptomatic; may present with seizures or focal neurologic signs.- Resection and/or radiosurgery. - Arachnoid cell origin.- Spindle cells concentrically arranged in a whorled pattern; psammoma bodies (laminated calcifications).
• Syringomyelia Cystic cavity within central canal of spinal cord (syringobulbia if in medulla). - Fibers crossing in anterior white commissure (spinothalamic tract) are typically damaged first. Results in a "cape-like," bilateral symmetrical loss of pain and temperature sensation in upper extremities (fine touch sensation is preserved).- Expansion of syrinx may damange corticospinal tract → bilateral flaccid paralysis and muscle atrophy. - Associated with Chiari I malformation, trauma, and tumors. - Most common at C8-T1.
• Acetylcholine Location of synthesis: Basal nucleus of Meynert ↓ Alzheimer disease ↓ Huntington disease ↑ Parkinson disease
• Dopaminergic pathways Mesocortical: ↓ activity → "negative" symptoms (eg, anergia, apathy, lack of spontaneity).- Antipsychotic drugs have limited effects. Mesolimbic: ↑ activity → "positive" symptoms (eg, delusions, hallucinations).- 1° therapeutic target of antipsychotic drugs. Nigrostriatal: ↓ activity → extrapyramidal symptoms (eg, dystonia, akathisia, parkinsonism, tardive dyskinesia).- Major dopaminergic pathway in brain. Tuberoinfundibular: ↓ activity → ↑ prolactin → ↓ libido, sexual dysfunction, galactorrhea, gynecomastia.
• Athetosis Slow, writhing, snake-like movements; especially seen in fingers. - Lesion in basal ganglia (eg, Huntington)
• Chorea Sudden, jerky, purposeless movements - Lesion in basal ganglia - Chorea = dancing- Seen in Huntington disease and in acute rheumatic fever (Sydenham chorea).
• Dystonia Sustained, involuntary muscle contractions - Writer's cramp, blepharospasm
• Tremor Essential tremor:- High-frequency tremor with sustained posture (eg, outstretched arms), worsened with movement or when anxious.- Often familial. Patients often self-medicate with alcohol, which ↓ tremor amplitude.- Treatment: nonselective β-blockers (eg, propanolol), primidone (barbiturate). Intention tremor:- Slow, zigzag motion when pointing/extending toward a target.- Cerebellar dysfunction. Resting tremor:- Uncontrolled movement of distal appendages (most noticeable in hands).- Tremor alleviated by intentional movement.- Lesion in substantia nigra.- Occurs at rest; "pill-rolling tremor" of Parkinson disease.
• Hemiballismus Sudden, wild flailing of 1 arm +/- ipsilatreal leg - Lesion in contralateral subthalamic nucleus (eg, lacunar stroke)
• Myoclonus Sudden, brief, uncontrolled muscle contraction Jerks, hiccups, common in metabolic abnormalities such as renal and liver failure
• Parkinson disease Degenerative disorder of CNS associated with Lewy bodies (composed of α-synuclein – intracellular eosinophilic inclusions) and loss of dopaminergic neurons (ie, depigmentation) of substantia nigra pars compacta. - Tremor (pill-rolling tremor at rest)- Rigidity (cogwheel)- Akinesia (or bradykinesia)- Postural instability- Shuffling gait MPTP, a contaminant in illegal drugs, is metabolized to MPP+, which is toxic to substantia nigra.
• Huntington disease Autosomal dominant trinucleotide (CAG)n repeat expansion in the huntingtin (HTT) gene on chromosome 4. Expansion of the protein's polyglutamine region results in a gain-of-function that leads to pathological interaction with other proteins, including repression transcriptional factors. - Abnormal huntingtin → ↑ histone deacetylation → silencing genes necessary for survival - Symptoms manifest between ages 20 and 50.- Characterized by choreiform movements, athetosis, aggression, depression, dementia. - ↑ dopamine ↓ GABA, ↓ ACh in brain.- Neuronal death via NMDA-R binding and glutamate excitotoxicity. - Atrophy of caudate and putamen with ex vacuo ventriculomegaly.
• Osmotic demyelination syndrome (central pontine myelinolysis) Massive axonal demyelination in pontine white matter 2° to osmotic changes, most commonly iatrogenic correction of hyponatremia but also rapid shifts of other osmolytes (eg, glucose). - Acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness.- Can cause "locked-in-syndrome." Correcting serum Na+ too fast:- "From low to high, your pons will die" (osmotic demyelination syndrome).- "From high to low, your brains will blow" (cerebral edema/herniation).
• Multiple sclerosis Autoimmune inflammation and demyelination of CNS (brain and spinal cord) with subsequent axonal damage. Can present with:- Acute optic neuritis (sudden unilateral visual loss of vision associated with Marcus Gunn pupil)- Brain stem/cerebellar syndromes (eg, diplopia, ataxia, scanning speech, intention tremor, nystagmus/INO (bilateral > unilateral)- Pyramidal tract weakness- Spinal cord syndromes (eg, electric shock-like sensation along spine on neck flexion [Lhermitte phenomenon], neurogenic bladder, paraparesis, sensory manifestations affecting the trunk or one or more extremity. - Symptoms may exacerbate with increased body temperature (eg, hot bath, exercise). - Relapsing and remitting is most common clinical course.- Most often affects women in their 20s and 30s; more common in Caucasians living farther from equator. Charcot triad of MS:1. Scanning speech2. Intention tremor3. Nystagmus Findings:- ↑ IgG level and myelin basic protein in CSF.- Oligocloncal bands are diagnostic.- MRI is gold standard: Periventricular plaques (areas of oligodendrocyte loss and reactive gliosis). Multiple white matter lesions disseminated in space and time. Treatment: Stop relapses and halt/slow progression with disease-modifying therapies (eg, β-interferon, glatiramer, natalizumab). Treat acute flares with IV steroids. Symptomatic treatment for neurogenic bladder (catheterization, muscarinic antagonists), spasticity (baclofen, GABAB receptor agonists), pain (TCAs, anticonvulsants).
• Acute inflammatory demyelinating polyradiculopathy Most common subtype of Guillain-Barré syndrome.Autoimmune condition associated with infections (eg, Campylobacter jejuni, viruses [eg, Zika]) that destroys Schwann cells by inflammation and demyelination of peripheral nerves (including cranial nerves III-XII) and motor fibers likely due to molecular mimicry, inoculations, and stress, but no definitive link to pathogens. Results in symmetric ascending muscle weakness/paralysis and depressed/absent DTRs beginning in lower extremities.- Facial paralysis (usually bilateral) and respiratory failure are common.- May see autonomic dysregulation (eg, cardiac irregularities, hypertension, hypotension) or sensory abnormalities.- Almost all patients survive; majority recover completely after weeks to months. - ↑ CSF protein with normal cell count (albuminocytologic dissociation). Treatment: Respiratory support, plasmapheresis, IV immunoglobulins. No role for steroids.
• Progressive multifocal leukoencephalopathy Demyelination of CNS due to destruction of oligodendrocytes (2° to reactivation of latent JC virus infection). - Seen in 2-4% of AIDS patients. - Rapidly progressive, usually fatal. - Predominantly involves parietal and occipital areas; visual symptoms are common. - ↑ risk associated with natalizumab, rituximab.
• Sturge-Weber syndrome (encephalotrigeminal angiomatosis) Congenital, non-inherited (sporadic), developmental anomaly of neural crest derivatives due to somatic mosaicism for an activating mutation in one copy of the GNAQ gene.  - Affects small (capillary-sized) blood vessels → port-wine stain of the face (nevus flammeus, a non-neoplastic "birthmark" in V1/V2 distribution)- Ipsilateral leptomeningeal angioma → seizures/epilepsy- Intellectual disability- Episcleral hemangioma → ↑ IOP → early-onset glaucoma STURGE-Weber: Sporadic, port-wine stain; Tram track calcifications (opposing gyri); Unilateral; Retardation; Glaucoma, GNAQ gene; Epilepsy
• Tuberous sclerosis TSC1 mutation on chromosome 9 or TSC2 mutation on chromosome 16. Tumor suppression genes.- Autosomal dominant, variable expression. - Hamartomas in CNS and skin- Angiofibromas- Mitral regurgitation- Ash-leaf spots (on trunk and extremities)- Cardiac rhabdomyoma (→ symptoms of congestive heart failure)- Intellectual disability- Renal angiomyolipoma- Seizures- Shagreen patches (in lumbosacral region)- ↑ incidence of subependymal giant cell astrocytomas - Ungual fibromas
• Neural development Notochord induces overlying ectoderm to differentiate into neurectoderm and form neural plate.Neural plate gives rise to neural tube and neural crest cells.Notochord becomes nucleus pulposus of intervertebral disc in adults. Alar plate (dorsal): sensoryBasal plate (ventral): motor
• Central and peripheral nervous system origins Neuroepithelia in neural tube – CNS neurons, ependymal cells (inner lining of ventricles, make CSF), oligodendrocytes, astrocytes. Neural crest – PNS neurons, Schwann cells. Mesoderm – Microglia (like macrophages).
• Neural tube defects Neuropores fail to fuse (4th week) → persistent connection between amniotic cavity and spinal canal. Associated with maternal diabetes as well as low folic acid intake before conception and during pregnancy. - ↑ α-fetoprotein (APF) in amniotic fluid and maternal serum (except spina bifida occulta = normal AFP).- ↑ acetylcholinesterase (AChE) in amniotic fluid is a helpful confirmatory test. Spina bifida occulta: Failure of caudal neuropore to close, but no herniation. Usually seen at lower vertebral levels. Dura is intact. Associated with tuft of hair or skin dimple at level of bony defect. Meningocele: Meninges (but no neural tissue) herniate through bony defect. Associated with spina bifida cystica. Meningomyelocele: Meninges and neural tissue (eg, cauda equina) herniate through bony defect. Myeloschisis: Also known as rashischisis. Exposed unfused neural tissue without skin/meningeal covering. Anencephaly: Failure of rostral neuropore to close → no forebrain, open calvarium. Clinical findings: polyhydramnios (no swallowing center).
• Holoprosencephaly Failure of left and right hemispheres to separate; usually occurs during weeks 5-6. - May be related to mutations in sonic hedgehog signaling pathway. - Moderate form has cleft lip/palate, most severe form results in cyclopia. - Seen in trisomy 13 and fetal alcohol syndrome. - MRI reveals monoventricle and fusion of basal ganglia.
• Posterior fossa malformations Chiari I malformation: Ectopia of cerebellar tonsils (1 structure). Congenital, usually asymptomatic in childhood, manifests in adulthood with headaches and cerebellar symptoms. Associated with spinal cavitations (eg, syringomyelia). Chiari II malformation: Herniation of low-lying cerebellar vermis and tonsils (2 structures) through foramen magnum with aqueductal stenosis → hydrocephalus. Usually associated with lumbosacral meningomyelocele (may present as paralysis/sensory loss at and below the level of the lesion). Dandy-Walker syndrome: Agenesis of cerebellar vermis leads to cystic enlargement of 4th ventricle that fills the enlarged posterior fossa. Associated with noncommunicating hydrocephalus, spina bifida.
• Sensory receptors Free nerve endings:- C – slow, unmyelinated fibers- Aδ – fast, myelinated fibers- All skin, epidermis, some viscera- Senses: pain, temperature Merkel discs:- Large, myelinated fibers; adapt slowly- Finger tips, superficial skin- Senses: pressure, deep static touch (eg, shapes edges), position sense Meissner corpuscles:- Large, myelinated fibers; adapt quickly- Glabrous (hairless) skin- Senses: dynamic fine/light touch, position sense Pacinian corpuscles: - Large, myelinated fibers; adapt quickly- Deep skin layers, ligaments, joints- Senses: vibration, pressure Ruffini corpuscles:- Dendritic endings with capsule; adapt slowly- Finger tips, joints- Senses: pressure, slippage of objects along surface of skin, joint angle changes
• Blood-brain barrier Prevents circulating blood substances (eg, bacteria, drugs) from reaching CSF/CNS. Formed by 3 structures:- Tight junctions between nonfenestrated capillary endothelial cells- Basement membrane- Astrocyte foot processes - Glucose and amino acids cross by carrier-mediated transport mechanisms.- Nonpolar/lipid-soluble substances cross rapidly via diffusion. No BBB:- Area postrema – vomiting after chemo- OVLT (organum vasculosum lamina terminalis) – osmotic sensing- Neurohypophysis – ADH release - Infarction and/or neoplasm destroys endothelial cell tight junctions → vasogenic edema.
• Hypothalamus Inputs (areas not protected by BBB): OVLT (senses change in osmolarity), area postrema (found in medulla, responds to emetics). Lateral area: Hunger. Destruction → anorexia, failure to thrive. Stimulated by ghrelin, inhibited by leptin. Lateral injury makes you Lean. Ventromedial area: Satiety. Destruction (eg, craniopharyngioma) → hyperphagia. Stimulated by leptin. Ventromedial injury makes you Very Massive. Anterior nucleus: Cooling, parasympathetic. Posterior nucleus: Heating, sympathetic. Suprachiasmatic nucleus: Circadian rhythm. Supraoptic and paraventricular nuclei: Synthesize ADH and oxytocin. Preoptic nucleus: Thermoregulation, sexual behavior. Releases GnRH. Failure of GnRH-producing hormones to migrate from olfactory pit → Kallmann syndrome.
• Sleep physiology Sleep cycle is regulated by the circadian rhythms, which is driven by suprachiasmatic nucleus (SCN) of hypothalamus. Circadian rhythm controls nocturnal release of ACTH, prolactin, melatonin, norepinephrine: SCN → norepinephrine release → pineal gland → melatonin. SCN is regulated by environment (eg, light).- Alcohol, benzodiazepines, and barbiturates are associated with ↓ REM sleep and delta wave sleep. Benzodiazepines are useful for night terrors and sleepwalking by ↓ N3 and REM sleep. Awake (eyes open): Beta (highest frequency, lowest amplitude)Awake (eyes closed): Alpha Non-REM sleep (75%)- N1 (5%, light sleep): Theta- N2 (45%, deeper sleep; when bruxism [teeth grinding] occurs): Sleep spindles and K complexes- N3 (25%, deepest non-REM sleep; when sleepwalking, night terrors, and bedwetting occus): Delta (lowest frequency, highest amplitude) REM sleep (25%)- Beta waves- Loss of motor tone, ↑ brain O2 use, ↑ and variable pulse and blood pressure ↑ ACh; when dreaming, nightmares, and penile/clitoral tumescence occur; may serve memory processing function.- Depression increases total REM sleep but decreases REM latency.- Extraocular movements due to activity of PPRF (paramedian pontine reticular formation).- Occurs every 90 minutes, and duration ↑ through the night.
• Thalamus Major relay for all ascending sensory information except olfaction. Ventral posteriolateral nucleus (VPL):- Spinothalamic and dorsal columns/medial lemniscus- Vibration, pain, pressure, proprioception, light touch, temperature- Destination: 1° somatosensory cortex Ventral posteriomedial nucleus (VPM):- Trigeminal and gustatory pathway- Face sensation, taste- Destination: 1° somatosensory cortex Lateral geniculate nucleus:- CN II, optic chiasm, optic tract- Vision- Destination: Calcarine sulcus Medial geniculate nuceus:- Superior olive and inferior colliculus of tectum- Hearing- Destination: Auditory cortex of temporal lobe Ventral lateral nucleus (VL):- Basal ganglia, cerebellum- Motor- Destination: Motor cortex
• Limbic system Collection of neural structures involved in emotion, long-term memory, olfaction, behavior modulation, ANS function. Consists of hippocampus, amygdalae, mammillary bodies, anterior thalamic nuclei, cingulate gyrus, entorhinal cortex.  Responsible for feeding, fleeing, fighting, feeling, and fucking (the famous 5 F's).
• Cerebellum Modulates movement; aids in coordination and balance. Input:- Contralateral cortex via middle cerebellar peduncle.- Ipsilateral proprioceptive information via inferior peduncle from spinal cord. Output: - The only output of cerebellar cortex = Purkinje cells (always inhibitory) → deep nuclei of cerebellum → contralateral cortex via superior cerebellar peduncle.- Deep nuclei (lateral → medial): Dentate - Emboliform - Globose - Fastigial Lateral lesions – affect voluntary movement of extremities; when injured, propensity to fall toward injured (ipsilateral) side.Medial lesions – involvement of midline structures (eg, vermal cortex, fastigial nuclei, flocculonodular lobe) → truncal ataxia (wide-based cerebellar gait), nystagmus, head tilting. Generally results in bilateral motor deficits affecting axial and proximal limb musculature.
• Basal ganglia Important in voluntary movements and making postural adjustments.Receives cortical input, provides negative feedback to cortex to modulate movement. Striatum = putamen (motor) + caudate (cognitive).Lentiform = putamen + globus pallidus. Direct (excitatory) pathway – SNc input stimulates the striatum, stimulating the release of GABA, which inhibits GABA release from the GPi, disinhibiting the thalamus via the GPi (↑ motion). Indirect (inhibitory) pathway – SNc input stimulates the striatum, releasing GABA that disinhibits STN via GPe inhibition, and STN stimulates GPi to inhibit the thalamus (↓ motion). Dopamine binds to D1, stimulating the excitatory pathway, and to D2, inhibiting the inhibitory pathway → ↑ motion.
• Vagal nuclei Nucleus solitarius: - Visceral sensory information (eg, taste, baroreceptors, gut distension)- Cranial nerves: VII, IX, X Nucleus ambiguus:- Motor innervation of pharynx, larynx, upper esophagus (eg, swallowing, palate elevation)- Cranial nerves: IX, X, XI (cranial portion) Dorsal motor nucleus:- Sends autonomic (parasympathetic) fibers to heart, lungs, upper GI- Cranial nerves: X
• Spinal nerves There are 31 pairs of spinal nerves in total: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal. Nerves C1-7 exit above corresponding vertebra. C8 spinal nerve exists below C7 and above T1. All other nerves exit below (eg, C3 exists above 3rd cervical vertebra; L2 enters below the 2nd lumbar vertebra). Vertebral disc herniation – nucleus pulposus herniates through annulus fibrosus; usually occurs posterolaterally at L4-L5 or L5-S1. Nerve usually affected is below the level of herniation (eg, L3-L4 disc spares L3 nerve and involves L4 nerve). Compression of S1 nerve root → absent ankle reflex.
• Landmark dermatomes C2: Posterior half of the skullC3: High turtleneck shirtC4: Low-collar shirtC6: Includes thumbsT4: At the nippleT7: At the xiphoid processT10: At the umbilicus. Important point of referred pain in early appendicitis.L1: At the inguinal ligamentL4: Includes the kneecapsS2, S3, S4: Sensation of penile and anal zones
• Common brain lesions Frontal lobe: Disinhibition and deficits in concentration, orientation, judgment; may have reemergence of primitive reflexes. Frontal eye fields: Eyes look toward (destructive) side of lesion. In seizures (irritative), eyes look away from side of the lesion. Paramedian pontine reticular formation: Eyes look away from side of lesion. Ipsilateral gaze palsy (inability to look toward side of lesion). Medial longitudinal fasciculus: Internuclear ophthalmoplegia (impaired adduction of ipsilateral eye; nystagmus of contralateral eye with abduction). Dominant parietal cortex: Agraphia, acalculia, finger agnosia, left-right disorientation → Gerstmann syndrome.Nondominant parietal cortex: Agnosia of contralateral side of the world → Hemispatial neglect syndrome. Hippocampus (bilateral): Anterograde amnesia – inability to make new memories. Basal ganglia: May result in tremor at rest, chorea, athetosis.  Subthalamic nucleus: Contralateral hemiballismus. Mammillary bodies (bilateral): Wernicke-Korsakoff syndrome – Confusion, ataxia, nystagmus, ophthalmoplegia, memory loss, confabulation, personality changes. Amygdala (bilateral): Klüver-Bucy syndrome – disinhibited behavior (eg, hyperphagia, hypersexality, hyperorality). Associated with HSV-1 encephalitis (temperal lobe). Dorsal midbrain: Parinaud syndrome – vertical gaze palsy, pupillary light-near dissociation, lid retraction, convergence-retraction nystagmus. Caused by stroke, hydrocephalus, pinealoma. Reticular activating system (midbrain): Reduced levels of arousal and wakefulness (eg, coma). Cerebellar hemisphere: Intention tremor, limb ataxia, loss of balance; damage to cerebellum → ipsilateral deficits; fall toward side of lesion. Red nucleus: Decorticate (flexor) posturing – lesion above red nucleus, presents with flexion of upper extremities and extension of lower extremities. Decerebrate (extensor) posturing – lesion at or below red nucleus, presents with extension of upper and lower extremities. Worse prognosis with decerebrate posturing. Cerebellar vermis: Truncal ataxia (wide-based, "drunken sailor" gait), dysarthria. Degeneration associated with chronic alcohol use.
• Ischemic brain disease/stroke Irreversible damage begins after 5 minutes of hypoxia. Most vulnerable: hippocampus, neocortex, cerebellum, watershed areas. Stroke imaging: noncontrast CT to exclude hemorrhage (before tPA can be given). CT detects ischemic changes in 6-24 hr. Diffusion-weighted MRI can detect ischemia within 3-30 mins. Histologic features:12-24 hours: Eosinophilic cytoplasm + pyknotic nuclei (red neurons)24-72 hours: Necrosis + neutrophils3-5 days: Macrophages (microglia)1-2 weeks: Reactive gliosis + vascular proliferation>2 weeks: Glial scar
• Epidural hematoma Rupture of middle meningeal artery (branch of maxillary artery), often 2° to skull fracture involving the pterion (thinnest area of the lateral skull). - Lucid interval. - Scalp hematoma and rapid intracranial expansion under systemic arterial pressure → transtentorial herniation, CN III palsy. - CT shows biconvex (lentiform), hyperdense blood collection not crossing suture lines.
• Subdural hematoma Rupture of bridging veins. - Can be acute (traumatic, high-energy impact → hyperdense on CT) or chronic (associated with mild trauma, cerebral atrophy, elderly, alcoholism → hypodense on CT). Also seen in shaken babies. - Predisposing factors: brain atrophy, trauma. - Crescent-shaped hemorrhage that crosses suture lines. - Can cause midline shift, findings of "acute on chronic" hemorrhage.
• Subarachnoid hemorrhage Bleeding due to trauma, or rupture of an aneurysm (such as a saccular aneurysm) or arteriovenous malformation.- Rapid time course. - Patients complain of "worst headache of my life." - Bloody or yellow (xanthochromic) spinal tap. - Vasospasm can occur due to blood breakdown or rebleed 3-10 days after hemorrhage → ischemic infarct; nimodipine used to prevent/reduce vasospasm. - ↑ risk of developing communicating and/or obstructive hydrocephalus.
• Intraparenchymal hemorrhage Most commonly caused by systemic hypertension. - Also seen with amyloid angiopathy (recurrent lobar hemorrhagic stroke in elderly), vasculitis, neoplasm. - May be 2° to reperfusion injury in ischemic stroke. - Hypertensive hemorrhages (Charcot-Bouchard microaneurysm) most often occur in putamen of basal ganglia (lenticulostriate vessels), followed by thalamus, pons, and cerebellum.
• Effects of strokes - Anterior circulation Mittel cerebral artery:- Area: Motor and sensory cortices – upper limb and face. Temporal lobe (Wernicke area); frontal lobe (Broca area).- Symptoms: Contralateral paralysis and sensory loss – face and upper limb. Aphasia if in dominant (usually left) hemisphere. Hemineglect if lesion affects nondominant (usually right) side.- Wernicke aphasia is associated with right superior quadrant visual field defect due to temporal lobe involvement. Anterior cerebral artery: - Area: Motor and sensory cortices – lower limb.- Symptoms: Contralateral paralysis and sensory loss – lower limb, urinary incontinence. Lenticulostriate artery: - Area: Striatum, internal capsule.- Symptoms: Contralateral paralysis. Absence of cortical signs (eg, neglect, aphasia, visual field loss).- Common location of lacunar infarcts, due to hyaline arteriosclerosis 2° to unmanaged hypertension.
• Aneurysms Saccular (berry) aneurysm: Occurs at bifurcations in the circle of Willis. Most common site is junciton of ACom and ACA. Associated with ADPKD, Ehlers-Danlos syndrome. Other risk factors: advanced age, hypertension, smoking, race (↑ in African-Americans).- Usually clinically silent until rupture → subarachnoid hemorrhage ("thunderclap headache") → focal neurologic deficits.- Can also cause symptoms via direct compression of surrounding structures by growing aneurysm.→ ACom–compression → bitemporal hemianopsia (compression of optic chiasm); visual acuity deficits; rupture → ischemia in ACA distribution → contralateral lower extremity hemiparesis, sensory deficits.→ MCA–rupture → contralateral upper extremity and facial hemiparesis, sensory deficits.→ PCom–compression → ipsilateral CN III palsy → mydriasis ("blown pupil"); may also see ptosis, "down and out" eye. Charcot-Bouchard microaneurysm: Common, associated with chronic hypertension; affects small vessels (eg, lenticulostriate arteries in basal ganglia, thalamus) and can cause lacunar strokes. Not visible on angiography.
• Seizures Characterized by synchronized, high-frequency neuronal firing. Variety of forms. Partial (focal) seizures: Affect single area of the brain. Most commonly originate in medial temporal lobe. Often preceded by seizure aura; can secondarily generalize. - Simple partial (consciousness intact) – motor, sensory, autonomic, psychic- Complex partial (impaired consciousness, automatisms) Generalized seizures: - Absence (petit mal) – 3 Hz spike-and-wave discharges, no postictal confusion, blank stare- Myoclonic – quick, repetitive jerks- Tonic-clonic (grand mal) – alternating stiffening and movement- Tonic – stiffening- Atonic – "drop" seizures (falls to floor); commonly mistaken for fainting Epilepsy – a disorder of recurrent seizuresStatus epilepticus – continuous (>5-30 min) or recurring seizures that may result in brain injury.

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