Neurology

Brief, reversible episode of focal neurologic dysfunction without acute infarction (⊝ MRI), with the majority resolving in <15 minutes; deficits due to focal ischemia.

Bleeding into ventricles.- Increased risk in premature and low-birth-weight infants. - Originates in germinal matrix, a highly vascularized layer within the subventricular zone. - Due to reduced glial fiber support and impaired autoregulation of BP in premature infants. - Can present with altered level of consciousness, bulging fontanelle, hypotension, seizures, coma.

Anterior spinal artery: - Lateral corticospinal tract → Contralateral paralysis – upper and lower limbs.- Medial lemniscus → ↓ contralateral proprioception.- Caudal medulla – hypoglossal nerve → Ipsilateral hypoglossal dysfunction.= Medial medullary syndrome – caused by infarct of paramedian branches of ASA and/or vertebral arteries. Posterior inferior cerebellar artery (PICA) (Lateral medulla):- Ncl. ambiguus (CN IX, X, XI) → Dysphagia, hoarseness, ↓ gag reflex, hiccups- Vestibular nuclei → Vomiting, vertigo, nystagmus- Lateral spinothalamic tract, spinal trigeminal nucleus → ↓ pain and temperature sensation from contralateral body; ipsilateral face- Sympathetic fibers → Ipsilateral Horner syndrome- Inferior cerebellar peduncle → Ipsilateral ataxia, dysmetria= Lateral medullary (Wallenberg) syndrome Anterior inferior cerebellar artery (Lateral pons):- Facial nucleus → Paralysis of face (LMN lesion vs UMN lesion in cortical stroke), ↓ lacrimation, ↓ salivation, ↓ taste from anterior 2/3 of tongue.- Vestibular nuclei: Vomiting, vertigo, nystagmus- Spinothalamic tract, spinal trigeminal tract → ↓ pain and temperature sensation from contralateral body, ipsilateral face- Sympathetic fibers → Ipsilateral Horner syndrome- Middle and inferior cerebellar peduncles → Ataxia, dysmetria- Labyrinthine artery → Ipsilateral sensorineural deafness, vertigo= Lateral pontine syndrome Basilar artery: - Pons, medulla, lower midbrain → RAS spared, therefore preserved consciousness- Corticospinal and corticobulbar tracts → Quadriplegia; loss of voluntary facial, mouth, and tongue movements- Ocular cranial nerve nuclei, paramedian pontine reticular formation → Loss of horizontal, but not vertical, eye movements= "Locked-in syndrome" Posterior cerebral artery: - Occipital lobe → Contralateral hemianopia with macular sparing; alexia without agraphia (dominant hemisphere).

Neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia on the contralateral side.  Occurs in 10% of stroke patients.

Caused by traumatic shearing forces during rapid acceleration and/or deceleration of the brain (eg, motor vehicle accident). Usually results in devastating neurologic injury, often causing coma or persistent vegetative state. MRI may show multiple lesions (punctate hemorrhages) involving the white matter tracts.

Aphasia – higher-order language deficit (inability to understand/produce/use language appropriately); caused by pathology in dominant cerebral hemisphere (usually left).Dysarthria – motor inability to speak (movement deficit). Repetition inpaired:- Broca (expressive): Nonfluent; comprehension intact. Patient appears fustrated, insight intact.- Wernicke (receptive): Fluent; comprehension impaired. Patients do not have insight.- Conduction: Fluent, comprehension intact. Can be caused by damage to arcuate fasciculus.- Global: Nonfluent; comprehension impaired. Arcuate fasciculus, Broca, and Wernicke areas affected. Repetition intact:- Transcortical motor: Nonfluent; comprehension intact. Affects frontal lobe around Broca area.- Transcortical sensory: Fluent; comprehension impaired. Affects temporal lobe around Wernicke area.- Transcortical, mixed: Nonfluent, comprehension impaired.

Children – genetic, infection (febrile), trauma, congenital, metabolic Adults – tumor, trauma, stroke, infection Elderly – stroke, tumor, trauma, metabolic, infection

Restlessness and intensive urge to move. Can be seen with neuroleptic use or as a side-effect of Parkinson treatment.

Extension of wrists cause "flapping" motion. Associated with hepatic encephalopathy, Wilson disease, and other metabolic derangements.

Worse at rest/nighttime. Relieved by movement. - Associated with iron deficiency, CKD.  - Treat with dopamine agonists (pramipexole, ropinirole).

Congenital degeneration of anterior horns of spinal cord. - LMN lesions only, symmetric weakness. - "Floppy baby" with marked hypotonia (flaccid paralysis) and tongue fasciculations. - Autosomal recessive inheritance mutation in SMN1 gene, which encodes a protein involved in assembly of small nuclear ribonucleoproteins (snRNPs) in lower motor neurons. Defective snRNP assembly results in impaired spliceosome function and degeneration of anterior horn cells in the spinal cord. - SMA type 1 is called Werdnig-Hoffmann disease.

CN V motor lesion: Jaw deviates toward side of lesion due to unopposed force from the opposite pterygoid muscle. CN X lesion: Uvula deviates away from side of lesion. Weak side collapses and uvula points away. CN XI lesion: Weakness turning head to contralateral side of lesion (SCM). Shoulder droop on side of lesion (trapezius). The left SCM contracts to help turn the head to the right. CN XII: LMN lesion. Tongue deviates toward side of lesion due to weakened tongue muscles on affected side.

- Bell palsy is the most common cause of peripheral facial palsy.  - Usually develops after HSV reactivation.- Other causes of peripheral facial palsy include Lyme disease, herpes zoster (Ramsay Hunt syndrome), sarcoidosis, tumors (eg, parotid gland), diabetes mellitus. - Treatment: corticosteorids ± acyclovir.- Most patients gradually recover function, but aberrant regeneration can occur. UMN lesion: - Lesion location: Motor cortex, connection from motor cortex to facial nucleus in pons- Affected side: Contralateral- Forehead spared, due to bilateral UMN innervation LMN lesion:- Lesion location: Facial nucleus, anywhere along CN VII- Affected side: Ipsilateral- Forehead affected- Incomplete eye closure (dry eyes, corneal ulceration), hyperacusis, loss of taste sensation to anterior tongue

↑ conduction velocity of signals transmitted down axons → saltatory conduction of action potential at the ndoes of Ranvier, where there are high concentrations of Na+ channels. Synthesis of myelin by oligodendrocytes in CNS (including CN I and II) and Schwann cells in PNS (including CN III-XII). Wraps and insulates axons: ↑ space constant and ↑ conduction velocity.

Acute neuronal injury (red neuron)- Type: Transient severe insult that leads to cell death- Schrinkage of the cell body- Pyknosis of the nucleus- Loss of Nissl substance- Eosinophilic cytoplasm Axonal reaction:- Type: Loss of axon- Enlargement of the cell body- Eccentric nucleus- Enlargement of the nucleolus- Dispersion of the Nissl substance Neuronal atrophy:- Type: Progressive degenerative disease- Loss of neurons and functional groups of neurons- Reactive gliosis