Neurology Flashcards
What drugs are used for essential tremor?
Beat blockers: propaolol and anticonvulsant: topiramate
What drugs are use in Parkinson’s Disease
L-dopa (decarboxylation of levodopa markedly increases the concentration of dopamine), amantadine (drug-induced extrapyrimadal side effects), selegeline and rasagaline (monoamine oxidase inhibitor (MAOI) that works by increasing the amount of dopamine in the brain), ropinirole and pramipexole (dopamine agonists), benzhexol (anticholinergic used in tremor dominant disease-side effects:memory disturbance and GI disturbance)
In what bacterial meningitis would a lymphocyte predominant CSF pattern be seen?
Listeria
Infarcts and visual field defects
Parietal- inferior homonymous quadrantopia
Temporal- superior homonymous quadrantopia
What type of tremor is cerebellar tremor
Intention tremor
What is another name for Pick’s Disease?
Frontotemporal dementia
Wernicke’s encephalopathy vs Korsakoff syndrome
Korsakoff syndrome is an abnormal mental state in which memory and learning due to nutritional deficiency in thiamine seen in alcohol dependence
Wernicke’s encephalopathy presents with confusion, ataxia, nystagmus and ophthalmoplegia
Retrograde vs antegrade amnesia
Anterograde amnesia
People with anterograde amnesia can’t form new memories, but they can still remember things from before they developed amnesia. Symptoms include forgetting conversations or events shortly after they happen, or forgetting the names and faces of people they met.
Retrograde amnesia
People with retrograde amnesia can’t recall memories from their past, including facts and general knowledge that they learned before the onset of amnesia. Symptoms include not being able to remember names, faces, places, dates, and other facts.
What is syringomelia?
Development of a cyst in the spinal cord. Can be post-traumatic. present with central cord syndrome involving the anterior horn (lower motor neurons), spinothalamic tract (pain and temperature), dorsal tracts are usually spared but may become involved
Types of seizures and presentation
Frontal lobe- prominent motor signs, speech arrest and dystonic posturing, laughing, crying
Parietal lobe- somatosensory phenomena
Occipital lobe- visual hallucinations
Temporal lobe- most common type of partial seizures. Staring, lip smacking and period of disorientation
Brainstem-myoclonus
Wallenburg Syndrome
Ischemia in Posterior inferior cerebellar artery leading to decreased sensation to ipsilateral half of face and contralateral limbs, ipsilateral Horner’s syndrome, ipsilateral weakness of the soft palate and pharynx, rotatory vertigo
Basilar artery stroke
motor and bulbar symptoms
Internal Carotid stroke
transient monocular blindness, hemodynamically variable symptoms
What does a basophilic adenoma produce?
ACTH, TSH, LH, FSH
Where is a craniopharyngioma located?
Craniopharyngiomas most frequently arise in the pituitary stalk and project into the hypothalamus. he most common presenting symptoms are headache (55–86%), endocrine dysfunction (66–90%), and visual disturbances (37–68%). Headache is slowly progressive, dull, continuous, and positional; it becomes severe in most patients when endocrine symptoms become obvious.
Brown-Sequard syndrome
ipsilateral weakness and loss of vibration and proprioception but contralateral loss of pain and temperature.
Causes penetrating injury to the spine, spinal tumor, infections, MS
Brain findings in different forms of dementia
Alzheimers- neurofibrillary tangles, senile plaques, amyloid deposits, hippocampus sclerosis
Huntington’s Disease- loss of neuronal cells particularly of the caudate and putamen
Lewy body dementia- Lewy bodies , neuronal bodies of aggregated proteins(alpha-synuclein), senile plaques
Pick’s disease (frontotemporal dementia)- round silver staining inclusions (Pick’s bodies), microvacuolation, swollen neurons, myelin and neuronal loss, astrocytic gloss
Dementia pugilistica (Chronic traumatic encephalopathy) “Punch-drunk syndrome” NFTS are seen. Seen in boxers and alcoholics
Charcot Marie Tooth Disease
Patients with Charcot-Marie-Tooth (CMT) disease have a significant family history. This history varies depending on the inheritance and penetrance pattern of the particular disorder (see Etiology). It is autosomal dominant. Spontaneous mutations also have been reported.
The age of presentation varies, depending on the type of CMT disease. Onset usually occurs in the first two decades of life.
Slowly progressing weakness beginning in the distal limb muscles is generally noted; it typically occurs in the lower extremities before it affects the upper ones. A subgroup of patients with CMT 1A may present with proximal muscle wasting and weakness.
Patients initially may complain of difficulty walking and frequent tripping due to foot and distal leg weakness. Frequent ankle sprains and falls are characteristic. Parents may report that a child is clumsy or simply not very athletic. As weakness becomes more severe, foot drop commonly occurs. Steppage (that is, gait in which the individual must lift the leg in an exaggerated fashion to clear the foot off of the ground) also is common.
Intrinsic foot muscle weakness commonly results in the foot deformity known as pes cavus. [38] Symptoms related to structural foot abnormalities include calluses, ulcers, cellulitis, and lymphangitis.
Hand weakness results in complaints of poor finger control, poor handwriting, difficulty using zippers and buttons, and clumsiness in manipulating small objects. Multidisciplinary assessment is warranted for evaluating impairment of manual function. [39] The hand may be affected at all ages in children with CMT 1A; hand problems in these patients may be underrecognized in the early stages of disease, causing potential delay in therapy. [40]
Patients usually do not complain of numbness. This may be because patients with CMT disease never had normal sensation and, therefore, simply do not perceive their lack of sensation.
Pain (musculoskeletal and neuropathic types) may be present. Muscle cramping is a common complaint. [41]
Autonomic symptoms usually are absent, but a few men with CMT disease have reported impotence.
Becker muscular dystrophy
Becker muscular dystrophy (BMD), initially described by Becker and Kiener in 1955, is an inherited disease with a male distribution pattern and a clinical picture similar to that of Duchenne muscular dystrophy (DMD).
It is X-linked, progressive muscle weakness
A typical developmental history of a patient with BMD may include the following:
Delayed gross motor milestones (eg, late walking, running, jumping, difficulty with stair climbing) may be reported
Initially, some children who are later diagnosed with BMD may be called clumsy
Increasing numbers of falls, toe walking, and difficulty rising from the floor may be later features
Proximal muscle weakness is reported
Subclinical cases may manifest later in life; dilated cardiomyopathy can be the first sign of BMD
Elbow contractures may be seen later in life
Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS) is the most common degenerative disease of the motor neuron system. Although ALS is incurable and fatal, with median survival of 3 years, treatment can extend the length and meaningful quality of life for patients.
Signs and symptoms
In 75–80% of patients, symptoms begin with limb involvement. Initial complaints in patients with lower limb onset are often as follows:
Tripping, stumbling, or awkwardness when running
Loss of lower extremity muscle bulk, strength, or endurance
Foot drop; patients may report a “slapping” gait
Initial complaints with upper limb onset include the following:
Reduced finger dexterity, cramping, stiffness, and weakness or wasting of intrinsic hand muscles
Wrist drop interfering with work performance
With bulbar onset (20–25% of patients), initial complaints are as follows:
Slurred speech, hoarseness, or decreased volume of speech
Aspiration or choking during a meal
Emotional difficulties in some ALS patients are as follows:
Involuntary laughing or crying
Depression
Impaired executive function and other cognitive changes
Behavioral changes
In lower motor neuron (LMN) involvement, fasciculations may occur early on in the disease, particularly in the tongue and limbs. Patients with upper motor neuron (UMN) involvement generally are hyperreflexic and stiff. Reflexes may be diminished due to LMN involvement. UMN symptoms may include spasms and sudden, uncontrolled straightening movements of the lower limbs.
In 75–80% of patients, symptoms begin with limb involvement, while 20–25% of patients present with bulbar symptoms. For those with limb involvement at presentation, the frequency of upper limb versus lower limb involvement is approximately equal.
Muscle biopsy is needed only rarely but may be considered if the presentation of ALS is atypical. The results will confirm the presence of signs of denervation and reinnervation or may lead to an alternative diagnosis, such as inclusion body myositis.
The presence of small, angular fibers is consistent with neurogenic atrophy (denervation). Fiber-type grouping is consistent with reinnervation.
Nerve conduction studies and needle electromyography (EMG) are useful for confirming the diagnosis of ALS and for excluding peripheral conditions that resemble ALS.
Features of vestibular schwannoma
unilateral hearing loss, trigeminal neuralgia, tinnitus, vertigo/dizziness
Progressive supra nuclear palsy
tendency to fall backwards with impairment of downward gaze with features of parkinson’s
Multiystem atrophy presents similar with postural hypotension
Wernicke’s encephalopathy triad
confusion, ataxia and ophthalmoplegia. Nystagmus may also be seen
Multiple sclerosis
There is intrathecal synthesis of IgG with the formation of oligoclonal bands. It affects white matter and there is usually abnormally visually evoked potentials.
Vestibular schwannoma
vestibulocochlear nerve. Presents with unilateral hearing loss, ipsilateral ataxia and facial weakness as well as loss of trigeminal sensation
