Extradural hemorhage - mnemonic

A-    Artery ( Middle meningeal artery) - cause

B-    Bi-
C-    Convex

D-    dural
E-    Extra-

Transdermal Rotigotine: A Clinically Innovative Dopamine-Receptor Agonist for the Management of Parkinson's Disease

Rotigotine is a highly lipophilic dopamine-receptor agonist and the first transdermally delivered agent to demonstrate efficacy and safety as monotherapy in early Parkinson's disease and to reduce “off” hours in levodopa-treated patients with advanced Parkinson's disease. The rotigotine pharmacophore is nonergolinic and demonstrates high affinity for dopamine D₂ and D₃ receptors. With once-daily application, the patch matrix provides continuous, nonfluctuating plasma drug levels at steady state, resulting in continuous and steady plasma and brain levels and striatal dopamine-receptor stimulation.

Read More: http://pharmacotherapyjournal.org/doi/abs/10.1592/phco.29.12.1452?cookieSet=1

Hyperkinetic Movement Disorders

Tremor Rhythmic oscillation of a body part due to intermittent muscle contractions Dystonia Involuntary patterned sustained or repeated muscle contractions often associated with twisting movements and abnormal posture. Athetosis Slow, distal, writhing, involuntary movements with a propensity to affect the arms and hands Chorea Rapid, semipurposeful, graceful, dance-like nonpatterned involuntary movements involving distal or proximal muscle groups Myoclonus Sudden, brief (<100 ms), jerk-like, arrhythmic muscle twitches Tic Brief, repeated, stereotyped muscle contractions that are often suppressible. Can be simple and involve a single muscle group or complex and affect a range of motor activities

Papez circuit

Papez circuit is a complex circuit involved in expression of emotions. It connects the limbic system with hypothalamus and thalamus.

Cavernous Sinus

Dural venous sinuses

The Lemon Sign

The lemon sign refers to the shape of the fetal skull at ultrasonography (US) when the frontal bones lose their normal convex contour and appear flattened or inwardly scalloped.
This gives the skull a shape similar to that of a lemon . The sign is seen on transverse sonograms of the fetal cranium obtained at the level of the ventricles.

The lemon sign has a strong association with spina bifida. Although the exact pathogenesis is unknown, it has been postulated that the decrease in the intraspinal pressure in neonates with spina bifida causes the brain to shift downward. This shift decreases the intracranial pressure, which is reflected onto the fetal cranium. The frontal bones are the most vulnerable to the decreased intracranial pressure and respond by flattening or scalloping inward. As the fetus matures, the lemon sign disappears because the frontal bones become stronger and are able to withstand the decreased pressure.




The lemon sign is not exclusive to spina bifida. It has been seen in a variety of conditions such as encephalocele, Dandy-Walker malformation with encephaloceles, thanatophoric dysplasia, cystic hygroma, diaphragmatic hernia, agenesis of the corpus callosum, fetal hydronephrosis, and umbilical vein varix and two-vessel cord

Determining the Level of the Lesion - Spinal Cord

The presence of a horizontally defined level below which sensory, motor, and autonomic function is impaired is a hallmark of spinal cord disease. This sensory level is sought by asking the patient to identify a pinprick or cold stimulus applied to the proximal legs and lower trunk and successively moved up toward the neck on each side. Sensory loss below this level is the result of damage to the spinothalamic tract on the opposite side one to two segments higher in the case of a unilateral spinal cord lesion, and at the level of a bilateral lesion. The discrepancy in the level of a unilateral lesion is the result of the course of the second-order sensory fibers, which originate in the dorsal horn, and ascend for one or two levels as they cross anterior to the central canal to join the opposite spinothalamic tract. Lesions that transect the descending corticospinal and other motor tracts cause paraplegia or quadriplegia with heightened deep tendon reflexes, Babinski signs, and eventual spasticity (the upper motor neuron syndrome). Transverse damage to the cord also produces autonomic disturbances consisting of absent sweating below the implicated cord level and bladder, bowel, and sexual dysfunction.

The uppermost level of a spinal cord lesion can also be localized by attention to the segmental signs corresponding to disturbed motor or sensory innervation by an individual cord segment. A band of altered sensation (hyperalgesia or hyperpathia) at the upper end of the sensory disturbance, fasciculations or atrophy in muscles innervated by one or several segments, or a muted or absent deep tendon reflex may be noted at this level. These signs also can occur with focal root or peripheral nerve disorders; thus, they are most useful when they occur together with signs of long tract damage. With severe and acute transverse lesions, the limbs initially may be flaccid rather than spastic. This state of "spinal shock" lasts for several days, rarely for weeks, and should not be mistaken for extensive damage to the anterior horn cells over many segments of the cord or for an acute polyneuropathy.

The main features of transverse damage at each level of the spinal cord are summarized below.

Cervical Cord

Upper cervical cord lesions produce quadriplegia and weakness of the diaphragm. Lesions at C4-C5 produce quadriplegia; at C5-C6, there is loss of power and reflexes in the biceps; at C7 weakness affects finger and wrist extensors and triceps; and at C8, finger and wrist flexion are impaired. Horner's syndrome (miosis, ptosis, and facial hypohidrosis) may accompany a cervical cord lesion at any level.

Thoracic Cord

Lesions here are localized by the sensory level on the trunk and by the site of midline back pain that may accompany the syndrome. Useful markers for localization are the nipples (T4) and umbilicus (T10). Leg weakness and disturbances of bladder and bowel function accompany the paralysis. Lesions at T9-T10 paralyze the lower—but not the upper—abdominal muscles, resulting in upward movement of the umbilicus when the abdominal wall contracts (Beevor's sign).

Lumbar Cord

Lesions at the L2-L4 spinal cord levels paralyze flexion and adduction of the thigh, weaken leg extension at the knee, and abolish the patellar reflex. Lesions at L5-S1 paralyze only movements of the foot and ankle, flexion at the knee, and extension of the thigh, and abolish the ankle jerks (S1).

Sacral Cord/Conus Medullaris

The conus medullaris is the tapered caudal termination of the spinal cord, comprising the lower sacral and single coccygeal segments. The distinctive conus syndrome consists of bilateral saddle anesthesia (S3-S5), prominent bladder and bowel dysfunction (urinary retention and incontinence with lax anal tone), and impotence. The bulbocavernosus (S2-S4) and anal (S4-S5) reflexes are absent. Muscle strength is largely preserved. 

By contrast, lesions of the cauda equina, the nerve roots derived from the lower cord, are characterized by low back and radicular pain, asymmetric leg weakness and sensory loss, variable areflexia in the lower extremities, and relative sparing of bowel and bladder function. Mass lesions in the lower spinal canal often produce a mixed clinical picture with elements of both cauda equina and conus medullaris syndromes. 

Special Patterns of Spinal Cord Disease

The location of the major ascending and descending pathways of the spinal cord are shown below:

 Most fiber tracts—including the posterior columns and the spinocerebellar and pyramidal tracts—are situated on the side of the body they innervate. However, afferent fibers mediating pain and temperature sensation ascend in the spinothalamic tract contralateral to the side they supply. The anatomic configurations of these tracts produce characteristic syndromes that provide clues to the underlying disease process.

Brown-Sequard Hemicord Syndrome

This consists of ipsilateral weakness (corticospinal tract) and loss of joint position and vibratory sense (posterior column), with contralateral loss of pain and temperature sense (spinothalamic tract) one or two levels below the lesion. Segmental signs, such as radicular pain, muscle atrophy, or loss of a deep tendon reflex, are unilateral. Partial forms are more common than the fully developed syndrome.

Central Cord Syndrome

This syndrome results from selective damage to the gray matter nerve cells and crossing spinothalamic tracts surrounding the central canal. In the cervical cord, the central cord syndrome produces arm weakness out of proportion to leg weakness and a "dissociated" sensory loss, meaning loss of pain and temperature sensations over the shoulders, lower neck, and upper trunk (cape distribution), in contrast to preservation of light touch, joint position, and vibration sense in these regions. Spinal trauma, syringomyelia, and intrinsic cord tumors are the main causes.

Anterior Spinal Artery Syndrome

Infarction of the cord is generally the result of occlusion or diminished flow in this artery. The result is extensive bilateral tissue destruction that spares the posterior columns. All spinal cord functions—motor, sensory, and autonomic—are lost below the level of the lesion, with the striking exception of retained vibration and position sensation.

Foramen Magnum Syndrome

Lesions in this area interrupt decussating pyramidal tract fibers destined for the legs, which cross caudal to those of the arms, resulting in weakness of the legs (crural paresis). Compressive lesions near the foramen magnum may produce weakness of the ipsilateral shoulder and arm followed by weakness of the ipsilateral leg, then the contralateral leg, and finally the contralateral arm, an "around-the-clock" pattern that may begin in any of the four limbs. There is typically suboccipital pain spreading to the neck and shoulders.

Intramedullary and Extramedullary Syndromes

It is useful to differentiate intramedullary processes, arising within the substance of the cord, from extramedullary ones that compress the spinal cord or its vascular supply. The differentiating features are only relative and serve as clinical guides. 

With extramedullary lesions, radicular pain is often prominent, and there is early sacral sensory loss (lateral spinothalamic tract) and spastic weakness in the legs (corticospinal tract) due to the superficial location of leg fibers in the corticospinal tract. 

Intramedullary lesions tend to produce poorly localized burning pain rather than radicular pain and to spare sensation in the perineal and sacral areas ("sacral sparing"), reflecting the laminated configuration of the spinothalamic tract with sacral fibers outermost; corticospinal tract signs appear later. 

Regarding extramedullary lesions, a further distinction is made between extradural and intradural masses, as the former are generally malignant and the latter benign (neurofibroma being a common cause). Consequently, a long duration of symptoms favors an intradural origin.

Spinal Cord Levels Relative to the Vertebral Bodies

Spinal Cord Level Corresponding Vertebral Body Upper cervical Same as cord level Lower cervical 1 level higher Upper thoracic 2 levels higher Lower thoracic 2 to 3 levels higher Lumbar T10-T12 Sacral T12-L1

Clinical Differentiation of the Major Dementias

Disease First Symptom Mental Status Neuropsychiatry Neurology Imaging AD Memory loss Episodic memory loss Initially normal Initially normal Entorhinal cortex and hippocampal atrophy FTD Apathy; poor judgment/insight, speech/language; hyperorality Frontal/executive, language; spares drawing Apathy, disinhibition, hyperorality, euphoria, depression May have vertical gaze palsy, axial rigidity, dystonia, alien hand, or MND Frontal, insular, and/or temporal atrophy; spares posterior parietal lobe DLB Visual hallucinations, REM sleep disorder, delirium, Capgras' syndrome, parkinsonism Drawing and frontal/executive; spares memory; delirium prone Visual hallucinations, depression, sleep disorder, delusions Parkinsonism Posterior parietal atrophy; hippocampi larger than in AD CJD Dementia, mood, anxiety, movement disorders Variable, frontal/executive, focal cortical, memory Depression, anxiety Myoclonus, rigidity, parkinsonism Cortical ribboning and basal ganglia or thalamus hyperintensity on diffusion/flair MRI Vascular Often but not always sudden; variable; apathy, falls, focal weakness Frontal/executive, cognitive slowing; can spare memory Apathy, delusions, anxiety Usually motor slowing, spasticity; can be normal Cortical and/or subcortical infarctions, confluent white matter disease

Abbreviations: AD, Alzheimer's disease; CBD, cortical basal degeneration; CJD, Creutzfeldt-Jakob disease; DLB, dementia with Lewy bodies; FTD, frontotemporal dementia; MND, motor neuron disease; PSP, progressive supranuclear palsy.

The Molecular Basis for Degenerative Dementia

Dementia Molecular Basis Causal Genes and (Chromosome) Susceptibility Genes Pathology AD Abeta <2% carry these mutations. APP (21), PS-1 (14), PS-2 (1) (most mutations are in PS-1) Apo EPSILON 4 (19)  Amyloid plaques, neurofibrillary tangles FTD Tau Tau exon and intron mutations (17) (about 10% of familial cases) Progranulin (17) (10% of familial cases) H1 tau haplotypes Tau inclusions, Pick bodies, neurofibrillary tangles   TDP-43 FUS     TDP-43 inclusions FUS inclusions DLB alpha-synuclein Very rare alpha-synuclein (4) (dominant) Unknown alpha-synuclein inclusions (Lewy bodies) CJD PrPSCproteins   Prion (20) (up to 15% of cases carry these dominant mutations) Codon 129 homozygosity for methionine or valine Tau inclusions, spongiform changes, gliosis

Administration of Intravenous Recombinant Tissue Plasminogen Activator (Rtpa) for Acute Ischemic Stroke (Ais)

Indication Contraindication Clinical diagnosis of stroke Onset of symptoms to time of drug administration <3 h CT scan showing no hemorrhage or edema of >1/3 of the MCA territory Age >18 years Consent by patient or surrogate Sustained BP >185/110 mm Hg despite treatment Platelets <100,000;  HCT <25%;  glucose <50 or >400 mg/dL Use of heparin within 48 h and prolonged PTT, or elevated INR Rapidly improving symptoms Prior stroke or head injury within 3 months; prior intracranial hemorrhage Major surgery in preceding 14 days Minor stroke symptoms Gastrointestinal bleeding in preceding 21 days Recent myocardial infarction Coma or stupor

Selection of Antiepileptic Drugs

Generalized-onset Tonic-Clonic	Focal	Typical Absence	Atypical Absence, Myoclonic, Atonic
First-Line
Valproic acid Lamotrigine Topiramate	Lamotrigine Carbamazepine Oxcarbazepine Phenytoin Levetiracetam	Valproic acid Ethosuximide	Valproic acid Lamotrigine Topiramate

Some Common Intensities on T1- and T2-Weighted MRI Sequences

			Signal Intensity
Image	TR	TE	CSF	Fat	Brain	Edema
T1W	Short	Short	Low	High	Low	Low
T2W	Long	Long	High	Low	High	High
FLAIR (T2)	Long	Long	Low	Medium	High	High

Abbreviations: CSF, cerebrospinal fluid; TE, interval between Rf pulse and signal reception; TR, interval between radiofrequency (Rf) pulses; T1W and T2W, T1- and T2-weighted.

Findings Helpful for Localization Within the Nervous System

	Signs
Cerebrum	Abnormal mental status or cognitive impairment Seizures Unilateral weakness and sensory abnormalities including head and limbs Visual field abnormalities Movement abnormalities (e.g., diffuse incoordination, tremor, chorea)
Brainstem	Isolated cranial nerve abnormalities (single or multiple) "Crossed" weakness and sensory abnormalities of head and limbs, e.g., weakness of right face and left arm and leg
Spinal cord	Back pain or tenderness Weakness and sensory abnormalities sparing the head Mixed upper and lower motor neuron findings Sensory level Sphincter dysfunction
Spinal roots	Radiating limb pain Weakness or sensory abnormalities following root distribution Loss of reflexes
Peripheral nerve	Mid or distal limb pain Weakness or sensory abnormalities following nerve distribution "Stocking or glove" distribution of sensory loss Loss of reflexes
Neuromuscular junction	Bilateral weakness including face (ptosis, diplopia, dysphagia) and proximal limbs Increasing weakness with exertion Sparing of sensation
Muscle	Bilateral proximal or distal weakness Sparing of sensation

^a

Features of Cerebellar Ataxia, Sensory Ataxia, and Frontal Gait Disorders

	Cerebellar Ataxia	Sensory Ataxia	Frontal Gait
Base of support	Wide-based	Narrow base, looks down	Wide-based
Velocity	Variable	Slow	Very slow
Stride	Irregular, lurching	Regular with path deviation	Short, shuffling
Romberg	+/–	Unsteady, falls	+/–
Heel shin	Abnormal	+/–	Normal
Initiation	Normal	Normal	Hesitant
Turns	Unsteady	+/–	Hesitant, multistep
Postural instability	+	+++	++++
			Poor postural synergies getting up from a chair
Falls	Late event	Frequent	Frequent

Features of Peripheral and Central Vertigo

Sign or Symptom	Peripheral (Labyrinth or Vestibular Nerve)	Central (Brainstem or Cerebellum)
Direction of associated nystagmus	Unidirectional; fast phase opposite lesiona	Bidirectional (direction-changing) or unidirectional
Purely horizontal nystagmus without torsional component	Uncommon	May be present
Purely vertical or purely torsional nystagmus	Never presentb	May be present
Visual fixation	Inhibits nystagmus	No inhibition
Tinnitus and/or deafness	Often present	Usually absent
Associated central nervous system abnormalities	None	Extremely common (e.g., diplopia, hiccups, cranial neuropathies, dysarthria)
Common causes	Benign paroxysmal positional vertigo, infection (labyrinthitis), vestibular neuritis, Ménière's disease, labyrinthine ischemia, trauma, toxin	Vascular, demyelinating, neoplasm

^a In Ménière's disease, the direction of the fast phase is variable.

^b Combined vertical-torsional nystagmus suggests BPPV.

Arnold Chiari malformation