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• Flecainide: Na channel blocker, restores sinus rhythm in atrial fibrillation,

but, C.I. in LVF, MI


• Sotalol, azimilide, milride: K channel blocker
• Amiodarone: multi channel blocker, belongs to all categories of Vaughen-
Williams Classification
• Atenolol:
• The Pain “Neuromatrix”: From the thalamic nuclei (VPL & VPM), the
pain is relayed to somato-sensory cortex and subcortical regions, as
amygdala, hypothalamus, periaqueductal grey, basal ganglia, and most
notably, the insula and anterior cingulate cortex
• Time course of onset neurological symptoms by : V EMI SD:
 Sec., Min., hours, days, weeks, months
 Vascular, Epilepsy, Migraine, Inflammation, Structural (space
occupying, edema, tumor), Degeneration (senile, metabolic, toxic etc)
• Seizures, due to synchronous electrical discharge of cortical neurons
• Migraine, due to slow (2–3 mm/ min) spreading of a depressive wave
across the cerebral cortex
• Residual symptoms such as numbness, weakness or blindness
• Dominant hemisphere: Language problems, such as, speech, reading,
writing, comprehension
• Non-dominant: visuospatial problems, such as, Neglect, denial,
inattention, apraxia (dressing)
• Brainstem symptoms…related to various cranial nerves and also
Symmetrical Distal limb weakness (poor grip etc.)
• Neuromuscular Junction: strength wax and wane; weakness worse at
end of day/on sustained action
• Proximal Limb weakness: Neuromuscular junction, Muscle
• Distal limb weakness: Brainstem, Nerve Root
• Acute phases of UMN lesions (stroke /spinal shock): flaccid tone and
depressed reflexes, (takes days / weeks for tone / reflexes to increase)
• Pyramidal Lesions:
• Upper limb – extensor weakness
• Lower limb – flexor weakness
• Frontal lobe damage: apathy or disinhibition; Broca’s area
• Parietal lobe:
• Dominant: reading, writing, calculation and Praxis,
• Non-dominant: visuospatial tasks; Anosognosia, lesions here may
result in spatial neglect, usually left side is ignored;
• Occipital Lobe:
• Cortical blindness with Macular sparing: allows reading vision
• Charles–Bonnet syndrome: formed visual hallucinations
• Anton syndrome: Subjective denial of visual loss
ataxia, rapidly progressive dementia & myoclonus
Visual hallucinations
BSECJD Tauopathies
PD+DLB=PDD
Frontal Release
Signs: Grasp Reflex

intracellular hyperphosphorylated & extracellular amyloid


FUS pathology
e4 allele Pick’s bodies
Lewy bodies
Rare autosomal dominant forms TDP-43 inclusions

Cholinesterase inhibitors
atrophy of the left posterior temporal and parietal lobes
PPRF, VIth nerve nucleus and MLF infarction

Damage to MLF
ipsilateral
geniculate ganglion opposite INO
left eye develops nystagmus in abduction Bilateral
right eye fails to adduct pathognomonic of MS
doll's eye reflex Parinaud syndrome
Failure of up-gaze

pupil-
sparing Pendular & Jerk

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