Neurologic Differential Diagnosis Flashcards

1
Q

Framework for neurological DDx

A
  • Based on the patient history, results of the neurological exam, & localization of anatomy to identify patient problems
  • Determine if appropriate to treat
  • Determine hypothesis generation related to movement related dysfunction
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2
Q

Step 1 of neurological DDx framework

A
  • Elicition of clinical facts derived from patient Hx & neurologic exam
  • Signs & Sx are interpreted in the context of the relevant anatomy & physiology
  • Goal is to generate a list of hypothesized lesion localizations that direct evaluation & special testing selection
  • Hx & neurologic evaluation results are interpreted & s/s are clustered into recognizable syndromes
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3
Q

Step 2 of neurological DDx framework

A
  • Localization of the lesion to determine an anatomical Dx
  • Identification of the part(s) of the nervous system that could most likely account for the complete patient presentation
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4
Q

Step 3 of neurological DDx framework

A
  • Anatomic Dx is combined with the temporal features of the disease: mode of onset, course of illness, relevant past medical & family Hx, lab findings
  • Establish a timeline
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5
Q

Describe a hypothetico-deductive reasoning strategy

A
  • Generation & verification of hypothesis are confirmed or negated on an ongoing basis as patient information & data is collected
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6
Q

Elicitation of clinical facts: Observation, Medical record, & Subjective

A
  • PMH and family history: risk factors
  • Drug history: antipsychotics, anti epileptics, benzodiazepines, statins, lithium, methotrexate, opioids
  • History of present illness (HPI): temporal factors
  • Imaging or other studies
  • Labs: antibody testing, lumbar puncture, B12 & folate levels, inflammatory markers (ESR & C-reactive protein), liver function tests, thyroid tests, complete blood count & basic metabolic panel, hemoglobin A1C & heavy metal screening
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7
Q

Emergency situations/immediate medical assistance required

A
  • Loss of consciousness or difficulty to arouse
  • Extreme confusion non consistent with premorbid status
  • Uncontrolled seizure activity
  • Acute infection with neurological signs (nuchal rigidity, intense localized back pain)
  • Rapid onset of focal neurological deficits suggesting stroke (BE FAST)
  • Spinal column instability
  • Nonresponsive autonomic dysreflexia
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8
Q

Urgent situations/referral required

A
  • Acute onset of neurologic signs such as incontinence, saddle paresthesia, abnormal reflexes
  • Progressive neurologic signs in known neurologic diagnosis that is not degenerative
  • Evidence of motor neuron disease: Fasciculation, atrophy, weakness in limbs or trunk not previously diagnosed
  • Change in autonomic status
  • Bulbar and other cranial nerve signs/symptoms (except acute onset)
  • Constant headache that worsens over time
  • TIA symptoms
  • Vertebral artery insufficiency
  • Neuro signs inconsistent with diagnosis
  • Signs/symptoms of systemic illness
  • Significant changes in personality or cognitive status
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9
Q

Patient signs/neurological considerations

A
  • Mental status
  • Cranial nerve function
  • Force production
  • DTR/pathological reflexes
  • Coordination
  • Gait
  • Sensory integrity
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10
Q

Describe cognition neurological signs

A
  • Memory: medial temporal lobes, hippocampus, amygdala
  • Language: dominant hemisphere (usually L)
  • Expressive aphasia: Broca’s area (frontal lobe)
  • Receptive aphasia: Wernicke’s area (temporal lobe)
  • Attention: frontal lobe
  • Perseveration: frontal lobe
  • Impulsivity: frontal lobe
  • Apraxia
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11
Q

Brain structures and functions

A
  • Frontal lobe (Broca’s area): initiation, judgement, memory, impulse control, sequencing, social behavior
  • Parietal lobe: sensory integration, awareness of body image & environment
  • Temporal lobe (Wernicke’s area): long term memory, auditory processing
  • Occipital lobe: visual field, color discrimination
  • Cerebral cortex: Motor cortex/motor homunculus = contralateral control of movement; Somatosensory cortex/sensory homunculus = contralateral perception of sensation; Visual cortex = contralateral perception of vision; Auditory cortex = bilateral reception of auditory input
  • Corpus callosum: facilitates communication between the right & left hemispheres of the brain
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12
Q

List the cortical functions

A
  • Cognition
  • Memory
  • Apraxia
  • Aphasia
  • Agnosia
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13
Q

Slide 15

A
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14
Q

Coordination deficits testing

A
  • Test joint position sense first (eyes open then closed)
  • If joint position sense is adequate test coordination: heel to shin, finger to nose, repeated movements
  • Unilateral: ipsilateral cerebellar syndrome
  • Bilateral: bilateral cerebellar syndrome
  • Truncal ataxia, gait ataxia, without limb incoordination = midline cerebellar syndrome
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15
Q

Slide 17

A
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16
Q

Timing/temporal factors

A
  • Establish a timeline
  • Review the timeline & note the following: abrupt or insidious onset, episodic or continuous presentation, exacerbation or remission, stable or progressive improvement/regression, age of onset
17
Q

Lab tests specific to neurological DDx

A
  • Lumbar puncture: analysis of cerebrospinal fluid (CSF), assists with Dx MS, Guillain-Barré syndrome, normal pressure hydrocephalus, meningitis, encephalitis
  • Electrophysiological studies: assists with Dx ALS, spinal muscular atrophy, peripheral neuropathy, myasthenia, graves, myopathy, brachial plexopathy
  • Imaging: CT, MRI, PET, angiography
  • Biopsies: brain, muscle, nerve, artery
  • Standard laboratory analysis discussed on slide 7
18
Q

Localization of findings

A
  • CNS vs PNS
  • UMN vs LMN
  • Specific location: basal ganglia (BG), cerebellum, cranial nerves, cognitive signs/symptoms (cognition, memory, apraxia, aphasia, agnosia), autonomic dysfunction
19
Q

Define agnosia and aphasia

A
  • Agnosia: inability to interpret sensations & hence recognize things
  • Aphasia: Wernicke’s area (L temporal lobe, comprehension) and Broca’s area (L frontal lobe, production)
20
Q

CNS vs PNS localization of weakness

A
  • PNS: spinal nerves, brachial plexus, peripheral nerves, lumbosacral plexus, cauda equina, conus medullaris, facial nerve (CN VII)
  • CNS: region of motor homunculus, primary motor cortex, descending motor pathways, brainstem, cervical spinal cord
21
Q

Localization of stiffness

A
  • Spasticity: descending motor pathways at the cortical brainstem, or spinal cord levels
  • Rigidity: basal ganglia
  • Hypertonicity: descending motor pathways especially the reticulospinal & corticospinal tracts
  • Hypotonicity: cerebellum, descending motor pathways, & spinal cord in the acute stage of injury
22
Q

Localization of sensory abnormality like joint position/vibration/fine discriminative touch and pain/temperature/crude touch

A
  • Joint position/vibration/fine discriminative touch: PNS = sensory receptors, ascending peripheral nerves, spinal nerves, trigeminal nerve; CNS = dorsal column medical lemniscus of spinal cord, brainstem, thalamus, primary somatosensory cortex
  • Pain/temperature/crude touch: PNS = sensory receptors, ascending peripheral nerves, spinal nerves, trigeminal nerve; CNS = anterolateral pathway of spinal cord, brainstem, thalamus, primary somatosensory cortex
23
Q

UMN versus LMN signs

A
  • UMN: weakness, NO atrophy except in chronic disuse, NO fasciculations, increased reflexes except in acute lesions, & increased tone except in acute lesions
  • LMN: weakness, atrophy, fasciculations, decreased reflexes, & decreased tone
24
Q

Patterns of weakness based on location of lesion

A
  • Cortex: contralateral face & body
  • Brainstem: ipsilateral face & contralateral body
  • SCI: level of the lesion or below
  • Root lesion: dermatomal/myotome pattern of the root
  • Polyneuropathy: distal loss greater than proximal loss
  • NMJ: patchy, decreased grip strength/endurance, face symptoms can be common
  • Myopathy: proximal loss greater than distal loss
25
Q

Central causes of sensory loss

A
  • Relate the lesion site to sensory distribution (homunculus)
  • Loss of certain modalities (pain/temp, vibration, light touch)
  • Loss of higher level perceptual functions: stereognosis, graphesthesia, extinction
26
Q

Peripheral causes of sensory loss

A
  • Peripheral nerve distribution (ex: LFCN)
  • Dermatome (spinal nerve root level)
  • Stocking glove (polyneuropathy, DM II)
27
Q

Cerebellum signs and symptoms

A
  • Dysmetria, DDK, hyper or hypometria
  • Nystagmus
  • Dysarthria
  • Ataxia
  • Difficulty with motor planning & learning
28
Q

Basal ganglia signs and symptoms

A
  • Bradykinesia
  • Hypokinesia
  • Athetosis/chorea
  • Tremor
  • Dystonia
29
Q

Brainstem signs and symptoms

A
  • Cardiorespiratory funciton
  • Provides sensory & motor innervation to face & neck
  • Passageway for ascending sensory tracts & descending motor pathways
  • Regulation of consciousness
  • Sleep/wake cycle
  • Autonomic control
30
Q

Spinal cord signs and symptoms

A
  • Bowel/bladder dysfunciton
  • Sexual funciton
  • Complete
  • Incomplete: anterior cord, central cord, Brown sequared
31
Q

What is the 3 step process

A
  • Step 1: patient history and neurological examination
  • Step 2: Localization of lesion that is based on the clinical findings
  • Step 3: Combining anatomic diagnosis with temporal features, timeline, and ongoing verification & refinement of hypotheses