Neurology – Charts

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CNS : *Cerebral Cortex Lesion* : Motor Findings
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– chronic contralateral corticospinal-type weakness and spasticity – flexion is stronger than extension in the arm – plantar flexion is stronger than dorsiflexion in the foot, and the leg is externally rotated at thehip
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CNS : *Cerebral Cortex Lesion* : Sensory Findings
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Contralateral sensory loss in the limbs and trunk on the same side as the motor deficits
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CNS : *Cerebral Cortex Lesion* : DTRs
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increased DTRs
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CNS : *Cerebral Cortex Lesion* : example of cause
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cortical stroke
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CNS : *Brainstem Lesion* : Motor Findings
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weakness and spasticity plus cranial nerve deficits such as diplopia and dysarthria
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CNS : *Brainstem Lesion* : Sensory Findings
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variable; no typical sensory findings
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CNS : *Brainstem Lesion* : DTRs
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increased DTRs
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CNS : *Brainstem Lesion* : Example of Cause
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brainstem stroke, acoustic neuroma
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CNS : *Spinal Cord Lesion* : Motor Findings
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weakness and spasticity affecting both sides causing paraplegia or quadriplegia depending on the level of injury
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CNS : *Spinal Cord Lesion* : Sensory Findings
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dermatomal sensory deficit on the trunk bilaterally at the level of the lesion and sensory loss from tract damage below the level of the lesion
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CNS : *Spinal Cord Lesion* : Deep Tendon Reflexes
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increased DTR
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CNS : *Spinal Cord Lesion* : examples of causes
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trauma, causing cord compression
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CNS : *Subcortical Gray Matter* : Basal Ganglia Lesion : Motor Findings
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slowness of movement (bradykinesia), rigidity, and tremor
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CNS : *Subcortical Gray Matter* : Basal Ganglia Lesion : Sensory Findings
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sensation not affected
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CNS : *Subcortical Gray Matter* : Basal Ganglia Lesion : Deep Tendon Reflexes
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DTR normal or low
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CNS : *Cerebellar Lesion* : Motor Findings
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hypotonia, ataxia, and other abnormal movements, including nystagmus, dysdiadochokinesis, and dysmetria
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CNS : *Cerebellar Lesion* : Sensory Findings
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sensation not affected
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CNS : *Subcortical Gray Matter* : Basal Ganglia Lesion : Examples of Causes
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parkinsonism
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CNS : *Cerebellar Lesion* : Deep Tendon Reflexes
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DTR normal or decreased
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CNS : *Cerebellar Lesion* : examples of causes
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cerebellar stroke, brain tumor
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PNS : *Anterior Horn Cell Lesion* : Motor Findings
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weakness and atrophy in a segmental or focal pattern; fasiculations
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PNS : *Anterior Horn Cell Lesion* : Sensory Findings
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sensation intact
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PNS : *Anterior Horn Cell Lesion* : Deep Tendon Reflexes
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DTR decreased
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PNS : *Anterior Horn Cell Lesion* : Examples of Causes
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polio, amyotrophic lateral sclerosis
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PNS : *Spinal Roots and Nerves Lesions* : Motor Findings
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weakness and atrophy in a root-innervated pattern; sometimes with fasiculations
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PNS : *Spinal Roots and Nerves Lesions* : Sensory Findings
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corresponding dermatomal sensory deficits
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PNS : *Spinal Roots and Nerves Lesions* : Deep Tendon Reflexes
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decreased DTRs
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PNS : *Spinal Roots and Nerves Lesions* : Examples of Causes
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herniated cervical or lumbar disc
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PNS : *Peripheral Nerve – Mononeuropathy* : Motor Findings
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weakness and atrophy in a peripheral nerve distribution; sometimes with fasiculations
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PNS : *Peripheral Nerve – Mononeuropathy* : Sensory Findings
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sensory loss in the pattern of that nerve
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PNS : *Peripheral Nerve – Mononeuropathy* : Deep Tendon Reflexes
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decreased DTR
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PNS : *Peripheral Nerve – Mononeuropathy* : examples of causes
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trauma
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PNS : *Peripheral Nerve – Polyneuropathy* : Motor Findings
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weakness and atrophy more distal than proximal; sometimes with fasiculations
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PNS : *Peripheral Nerve – Polyneuropathy* : Sensory Findings
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sensory deficits, commonly in stocking-glove distribution
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PNS : *Peripheral Nerve – Polyneuropathy* : Deep Tendon Reflexes
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decreased deep tendon reflexes
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PNS : *Peripheral Nerve – Polyneuropathy* : Examples of Causes
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peripheral polyneuropathy of alcoholism, diabetes
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PNS : *Neuromuscular Junction Lesion* : Motor Findings
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fatigability more than weakness
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PNS : *Neuromuscular Junction Lesion* : Sensory Findings
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sensation intact
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PNS : *Neuromuscular Junction Lesion * : Deep Tendon Reflexes
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normal DTRs
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PNS : *Neuromuscular Junction Lesion* : Examples of Causes
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Myasthenia Gravis
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PNS : *Muscle Lesion* : Motor Findings
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weakness usually more proximal than distal; fasiculations rare
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PNS : *Muscle Lesion* : Deep Tendon Reflexes
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normal or decreased DTRs
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PNS : *Muscle Lesion* : Examples of Causes
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muscular dystrophy
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Anterior Cerebral Artery
Anterior Cerebral Artery
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pink part
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Anterior Choroidal Artery
Anterior Choroidal Artery
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yellow part
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Middle Cerebral Artery
Middle Cerebral Artery
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green part
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Posterior cerebral artery
Posterior cerebral artery
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purple part
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Prefrontal area
Prefrontal area
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yellow part
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Premotor area
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light blue part
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Primary Motor Cortex
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light purple area
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Motor speech (Broca’s) area
Motor speech (Broca's) area
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dark purple area
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Primary Somatic Sensory Cortex
Primary Somatic Sensory Cortex
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Dark Green area
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Somatic Sensory Association Area
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Middle green area
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Taste area
Taste area
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yellowish green area
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Primary Auditory Cortex
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light pinkish area
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Auditory Association Area
Auditory Association Area
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Violet area
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Sensory Speech (Wernicke’s area)
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orange area
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Reading comprehension area
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teal area
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Visual association area
Visual association area
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middle pink area
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Visual cortex
Visual cortex
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red area
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Vasodepressor or Vaovagal Syncope
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– sudden peripheral vasodilation esp in skeletal muscles without compensatory risk in cardiac output; heart rate then blood pressure fall; often slow onset, slow offset – brought on by a strong emotion such as fear or pain – predisposing factors : fatigue, hunger, a hot humid environment are – prodromal manifestations : restlessness, weakness, pallor, nausea, salivation, sweating, yawning – prompt return of consciousness when lying down but pallor weakness nausea and slight confusion may persist for a time
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Orthostatic (Postural) Hypotension
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– Inadequate vasocontrictor reflexes in both arterioles and veins, with resultant venous pooling, decreasing cardiac outpat, and low blood pressure – brought on by standing up – parkinsons, shy-drager syndrome, lewy body disease diabetes, amyloidosis, antihypertensive vasodilator drugs; prolonged bed rest are predisposing factors – associated with light headdedness and palpitations on standing up – improvement with lying down
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Cough Syncope
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– neurally mediated, possible vagal stimulation – brought on by severe paroxysm of coughing – chronic bronchitis in a muscular man is a predisposing factor – no prodromal manifestations except for cough – prompt return to normal
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Micturation Syncope
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– vasovagal stimulation – brought on by emptying the bladder after getting out of bed to void – predisposing factors include nocturia – prompt return to normal
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Arrhythmias
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– decreased cardiac output from cardiac ischemia, ventricular arrhythmias, prolonged QT syndrome, persistent bradycardia, infrafasicular block; often sudden onset; sudden offset – precipitating factors include sudden change in rhythm – predisposing factors include heart disease, aging decrease tolerance of abnormal rhythms – prompt return to normal prolonged cerbral hypoperfusion cardiac arrest
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Aortic Stenosis and Hypertrophic Cardiomyopathy
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– vascular resistance falls with exercise, but cardiac output cannot rise due to outflow obstruction – precipitating factors include exercise – predisposing factors include cardiac disorders – usually prompt return to normal
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Myocardial Infarction
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– sudden arrhythmia or decreased cardiac output – predisposing factors include coronary artery disease – prodromal manifestation is ischemic chest pain
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Massive Pulmonary Embolism
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– sudden hypoxia or decreased cardiac output – variable precipitating factors including prolonged bed rest and clotting disorders – DVT, bedrest, hypercoagulable states (SLE; cancer), protein S or C deficiency, antithrombin III deficiency, estrogen therapy – dyspnea, pleuritic chest pain are prodromal manifestations – recovery is related to time to diagnosis and treatment
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Hypocapnia due to Hyperventilation
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– constriction of cerebral blood vessels secondary to hypocapnia induced by hyperventilation – precipitating factors : anxiety and panic disorders – predisposing factors : anxiety – dyspnea, palpitations, chest discomfort, numbness and tingling of the hands and around the mouth lasting for several minutes, consciousness is often maintained – slow improvement as hyperventilation ceases
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Hypoglycemia
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– insufficient glucose to maintain cerebral metabolism; secretion of epinephrine contributes to symptoms; true syncope is uncommon – variable precipitating factors including fasting – insulin therapy and a variety of metabolic disorders are predisposing factors – sweating, tremor, palpitations, hunger, headache, confusion, abnormal behavior, coma are prodromal
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Hysterical Fainting from Conversion Reaction
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– brought on through stressful situation – hysterical personality traits are predisposing factors
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Jacksonian Seizures
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– tonic and then clonic movements that start unilaterally in the hand, foot, or face and spread to other body parts on the same side – normal consciousness
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Other motor focal seizures
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– turning of the head and eyes to one side, or tonic and clonic movements of an arm or leg without the Jacksonian spread – normal consciousness
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Focal Seizures with autonomic symptoms
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– a “funny feeling” in epigastrium, nausea, pallor, flushing, lightheadedness – normal consciousness
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Focal Seziures with subjective sensory or psychic phenomena
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– numbness, tingling, simple visual, auditory, or olfactory hallucinations such as flashing lights, buzzing, or odors – anxiety or fear; feelings of familiarity or unreality; dreamy states; fear or rage; flashback experiences; hallucinations – normal consciousness
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Focal Seizures with Impairment of Consciousness
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– the seizure may or may not start with autonomic or psychic symptoms – consciousness impaired and confusion – automatisms included chewing, smacking the lips, walking about and unbuttoning clothes – the patient may remember initial autonomic or psychic symptoms (aura) but is amnesic for the rest of the seizure
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Focal Seizures that become generalized
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– partial seizures that become generalized resemble tonic-clonic seizures; patient may not recall the focal onset – recollection of an aura and unilateral neurologic deficit during the postictal period
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Tonic Clonic (grand mal) Seizures : Clinical Manifestations
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– sudden loss of consciousness sometimes with a cry – body stiffens into tonic extensor rigidity – breathing stops and the person becomes cyanotic – clonic phase of rhythmic muscular contraction follows – breathing resumes and is often noisy with excessive dalivation
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Generalized Seizures : Postictal State
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confusion, drowsiness, fatigue, headache, muscular aching, and sometimes the temporary persistence of bilateral neurologic deficits such as hyperactive reflexes amnesia of the seizure and no recollection of aura
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Absence Seizures : Clinical Manifestations
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sudden brief lapse of consciousness with momentary blinking, staring, or movements of lips and hands but no failing – typical lasts less than 10 seconds and stop abruptly – atypical may last more than 10 seconds
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Absence Seizures : Postictal State
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no aura recalled
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Myoclonic Seizures : Clinical Manifestations
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sudden, brief rapid jerks, involving the trunk or limbs
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Myoclonic Attack : Clinical Manifestations
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sudden loss of consciousness with falling but no movements; injury may occur
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Myoclonic Attack : Postictal State
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either a prompt return to normal or brief period of confusion
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Resting (Static) Tremors
Resting (Static) Tremors
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prominent at rest and may decrease or disappear with voluntary movement; common, relatively slow, fine, pill-rolling tremor of parkinsonism, about 5 per second
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Postural Tremors
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appear when affected part is actively maintaining a posture; examples include the fine rapid tremor of hyperthyroidism, anxiety, fatigue
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Intention Tremors
Intention Tremors
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absent at rest, appear with movement and often get worse as the target gets closer; include disorders of cerebellar pathways, as in MS, or any other disease of the cerebellum
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Oral-Facial Dyskinesias
Oral-Facial Dyskinesias
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rhythmic, repetitive, bizarre movements that chiefly involve the face, mouth, jaw, and tongue; grimacing, pursing of the lips, protrusions of the tongue, opening and closing of the mouth, and deviations of the jaw
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Tics
Tics
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brief, repetitive, stereotyped coordinated movements occurring at irregular intervals i.e., tourette’s
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Dystonia
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grotesque twisted postures may result
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Athetosis
Athetosis
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slower more twisting and writhing movements that have a large amplitude; commonly involve the face and distal extremities
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Chorea
Chorea
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brief, rapid, jerky, irregular, and unpredictable; occur at rest or interrupt normal coordinated movements; they seldom repeat themselves; face, head, lower arms, and hands are often involved
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Wernicke’s Aphasia
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– fluent often rapid and effortless speech – inflection and articulation are good but sentences lack meaning and words are gibberish – may be totally incomprehensible – word comprehension, repetition, naming, reading comprehension, writing all impaired – lesion located in posterior superior temporal lobe
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Broca’s Aphasia
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– nonfluent – slow with few words and laborious effort – inflection and articulation are impaired but words are meaningful – small grammatical words often dropped – fair word and reading comprehension – impaired repetition, writing, and naming – lesion located in posterior inferior frontal lobe
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Nystagmus
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rhythmic oscillation of eyes; caused by vision impairment early in life, disorders of the labyrinth and cerebellar system, and drug toxicity; can occur normally when watching rapidly moving objects
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Nystagmus – Lateral Gaze
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nystagmus may be present in all directions but only accentuates in deviation of eyes as seen in extreme lateral gaze left or right; normal people show signs of slight nystagmus in lateral gaze
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Left-beating nystagmus
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if eyes jerk quickly to patients left and slowly to the right
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Pendular nystagmus
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nystagmus consisting only of coarse oscillations without quick and slow components
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Horizontal nystagmus
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Vertical nystagmus
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Rotary Nystagmus
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CN VII Peripheral Lesion
CN VII Peripheral Lesion
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paralyzes the entire right side of the face including forehead; right eye does not close and the eyeball rolls up; forehead not wrinkled and eyebrow not raised
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CN VII Central Lesion
CN VII Central Lesion
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Eye closes with slight weakness and forehead is wrinkled with eyebrow raised
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Lesions Producing Spastic Muscle Tone
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Upper motor neuron or corticospinal tract systems
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Spasticity
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– increased muscle tone that is greater when passive movement is rapid and less when passive movement is slow; greater at the extremes or movement arc; sudden limb reflexes – seen in stroke
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Lesions Producing Rigid Muscle Tone
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Basal Ganglion System
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Lead Pipe Rigidity
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increased resistance that persists throughout the movement arc independent of rate of movement
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Cogwheel Rigidity
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rigidity with flexion and extension of the wrist and forearm, a superimpose rachetlike jerkiness seen in parkinson’s patients
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Lesions Producing Flaccid Muscle Tone
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lower motor neuron system (from anterior horn cell to peripheral nerves)
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Flaccidity
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loss of muscle tone causing loose and floppy limbs; limbs may be hyperextensible or even flail like seen in Guillain Barre syndrome
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Lesions producing paratonia muscle tone
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both hemispheres, usually in the frontal lobes
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Paratonia
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sudden change in tone with passive ROM
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Paratonia – Mitghen
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sudden loss of tone that increases the ease of motion
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Paratonia – Gegenhalten
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sudden increase in tone making motion more difficult
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Spastic Hemiparesis
Spastic Hemiparesis
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– corticospinal tract lesion in stroke – poor control of flexor muscles during swing phase – arm is flexed, immoble, and held close to side with elbow, wrists, and interphalangeal joints flexed – leg extensors spastic – ankle plantar flexed and inverted – pts may drag toe, circle leg stiffly outward and forward or lean trunk to contralateral side to clear affected leg during walking
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Scissors Gait
Scissors Gait
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– spinal cord disease – caused by bilateral lower extremity spasticity including adductor spasm and abnormal proprioception – stiff gait with slow leg advancement – thighs tend to cross forward on each other with each step – steps are short – pts appear to be walking through water – common in cerebral palsy
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Steppage Gait
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– foot drop – secondary to peripheral motor unit disease – pts drag the feet or light them high with knees flexed and slap them down onto the floor – walking up stairs – cannot walk on heels – tibalis anterior and toe extensors are weak
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Parkinsonian Gait
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– basal ganglia defects – posture is stooped with flexion of head, arms, hips, and knees – pts are slow getting started – short shuffling steps with involuntary hastening – limited arm swings
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Cerebellar Ataxia
Cerebellar Ataxia
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– dx of cerebellum or associated tracts – gait is staggering, unsteady, and wide based with exaggerated difficulty on turns – pts cannot stand steadily w feet together whether eyes are opened or closed – nystagmus, dysmetria, and intention tremor
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Sensory Ataxia
Sensory Ataxia
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– loss of position sense in legs – gait is unsteady and wide based – pts throw their feet forward and outward and bring them down first on heels then on toes with double tapping sound – watch grown – with eyes closed they cannot stand steadily with feet together (positive Romberg)
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Toxic Metabolic Comas
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arousal centers poisoned or critical substrates depleted
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Toxic Metabolic Comas : Respiratory Pattern
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if regular may be normal or hypervenilation; if irregular usually Cheyne-Stokes
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Toxic Metabolic Comas : Pupillary size and reaction
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– equal and reactive to light – pinpoint = opiates/cholinergics; need magnifying glass to see reaction – fixed and dilated = anticholinergics/hypothermia
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Toxic Metabolic Comas : Causes
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– uremia – hyperglycemia – alcohol – drugs – liver failure – hypothyroidism – hypoglycemia – anoxia – ischemia – meningitis – encephalitis – hyperthermia – hypothermia
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Structural Coma
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lesion destroys or compresses brainstem arousal areas either directly or secondary to more distant expanding mass lesions
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Structural Coma : Respiratory Pattern
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– irregular especially Cheyne-Strokes or ataxic breathing
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Structural Coma : Pupillary Size and Reaction
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– unequal or unreactive to light – midposition, fixed = midbrain compression – dilated, fixed = compression of CN III from herniation
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Structural Coma : Causes
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– epidural, subdural, or intracerebral hemorrhage – cerebral infarct or embolus – tumor or abscess – brainstem infarct, tumor, or hemorrhage – cerebellar infarct, hemorrhage, tumor, or abscess
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Glasgow Coma Scale
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higher number = more aware
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Bilaterally Small Pupils
Bilaterally Small Pupils
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– 1-2.5 mm – suggest damage to the sympathetic pathways in the hypothalamus or metabolic encephalopathy – diffuse failure of cerebral function that has many causes including drugs – light reactions are usually normal
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Pinpoint Pupils
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– <1mm – suggests a hemorrhage in the pons or the effects of morphine, heroin, or other narcotics – light reaction may be seen w magnifying glass
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Midposition Fixed Pupils
Midposition Fixed Pupils
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– slightly dilated and fixed to light – suggest structural damage in the midbrain
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Bilaterally fixed and dilated pupils
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– may be due to severe anoxia and its sympathomimetic effects as seen after cardiac arrest – may also be seen from atropinelike agents, phenothiazines, or tricyclic antidepressants
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Bilaterally large reactive pupils
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may be due to cocaine, amphetamine, LSD or other sympathetic nervous system agonists
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One Large Pupil
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herniation of the temporal lobe causing compression of the oculomotor nerve and midbrain; most commonly seen in diabetic pts with infarction of CN III
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Decorticate Rigidity (Abnormal Flexor Response)
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– upper arms are flexed tight to the sides with elbows, wrists, and fingers flexed – legs are extended and internally rotated – feet are plantar flexed – implies a destructive lesion of the corticospinal tracts within or very near the cerebral hemispheres – when unilateral = chronic spastic hemiplegia
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Hemiplegia (Early)
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– sudden unilateral brain damage involving the corticospinal tract – one-sided paralysis – flaccid in early course with spasticity developing larger – paralyzed arm and leg are slack falling loosely without tone – spontaneous movements or responses are limited to opposite side – leg may lie externally rotated – one side of lower face is paralyzed and that cheek puffs on expiration – both eyes may be turned away from paralyzed side
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Decerebrate Rigidity (Abnormal Extensor Response)
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– jaws are clenched and neck is extended – arms are adducted and stiffly extended at the elbows with forearms pronated, wrists and fingers flexed – legs are stiffly extended at the knees with feet plantar flexed – may occur spontaneously or only in response to external stimuli (light, noise, or pain) – caused by a lesion in diencephalon, midbrain, or pons OR by metabolic disorders such as hypoxia and hypoglycemia

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