Brain lesions
|
Intracranial mass
[24]
[25]
|
-
Associated symptoms of brain tumors vary widely depending up location and size of
tumor
-
Symptoms and signs of increased ICP
-
Local mass effect causes headaches, seizures, nausea, ataxia, and cognitive dysfunction,
focal neurological deficits
-
Generalized mass effect presents as headache, nausea and vomiting, blurring of vision
-
Weakness is UMN/spastic pattern (upper limb extensors, lower limb flexors)
-
Brain abscess also presents with similar features along with fever
|
|
|
-
Consider steroids for peritumoral vasogenic edema
-
Manage raised ICP in the standard step-wise approach
-
Manage blood pressure and treat coagulopathy if there is intracranial bleed
-
Brain abscesses require targeted antimicrobial treatment and sometimes drainage
-
Surgical evacuation and excision of lesion if indicated
|
Acute ischemic stroke
|
|
-
UMN type
-
On the opposite side of lesion
-
Extensor > flexors in UL
-
Flexors > extensors in LL
-
Reflexes increased and plantar extensors on the side of hemiparesis
|
-
CT head
-
MRI brain (diffusion-weighted images)
-
Angiogram of neck and intracranial vessels
-
ECG/Echocardiography to rule out cardio-embolic cause
|
|
Postictal Todd’s paresis
[26] [27]
|
|
-
Transient weakness
-
Weakness varies widely in location, severity, duration, tone reflexes, and sensory
involvement
|
CT head to exclude other causes of weakness
|
|
Hypertensive encephalopathy
[28] [29]
|
-
Long standing, poorly controlled hypertension
-
Poor compliance with antihypertensive agents,
-
Headaches, confusion, visual disturbances, nausea, and vomiting
|
-
Severe, sustained hypertension
-
Transient, migratory neurological non-focal deficits, ranging from nystagmus to weakness,
and an altered mental status, ranging from confusion to coma
-
Funduscopic may reveal f/s/o HTN retinopathy—papilledema, hemorrhage, exudates, and
cotton wool spots
|
-
CT head
-
Urine toxicology screen
-
Coagulation profile
|
-
Invasive BP monitoring
-
IV antihypertensive agent
-
Aim to reduce initial MAP by no more than 25%
-
Avoid lowering BP too much, too quickly, as it may lead to cerebral ischemia
|
Hemiplegic migraine
[30] [31]
|
-
Start in the first or second decade of life as sporadic or familial
-
Most patients also have attacks of migraine with typical aura without weakness
-
Aura consists of a fully reversible motor weakness
-
Weakness may resolve before the headache starts or may persist for days
-
May be accompanied by ipsilateral numbness or tingling, with or without a speech disturbance
-
In familial hemiplegic migraine (FHM), there is positive family history in at least
one first- or second- degree relative
|
|
-
Diagnosis of exclusion
-
CT or MRI to exclude other etiologies
-
Angiography to rule out transient ischemic attacks and vascular abnormality
-
SPECT scan may show hypoperfusion during the aura phase
-
Genetic testing is available for FHM
|
-
Early neurologist involvement
-
Antiemetics, nonsteroidal anti-inflammatory drugs, and nonnarcotic pain relievers
-
Prophylactic treatment may include lamotrigine and acetazolamide
|
Spinal cord lesions
|
Spinal cord infarction
[32]
|
-
Acute quadriparesis or paraparesis with a sensory level corresponding with level of
cord infarct
-
No history of trauma or infection
-
60% of patients present with pain that localizes to the level of injury
-
May be associated with aortic surgery or procedures such as celiac ganglion ablation
-
May be having risk factors leading to hypercoagulable states
|
-
May present with anterior or posterior spinal artery syndrome (A/PSAS) depending upon
the portion of spinal cord involvement
-
ASAS: loss of motor power, usually bilateral weakness, occasionally unilateral
Initially flaccid paralysis and loss of deep tendon reflexes
Loss of pain/temperature sensation
Total anesthesia at the level of injury
|
-
MRI: Ischemic lesion matching an arterial territory of the cord
-
Spinal angiogram: as suggested from MRI to rule out malformations
-
Other investigations to rule out hypercoagulable state: prothrombotic and vasculitis screen
Toxicology screen
Electrocardiography
Echocardiography
Duplex ultrasonography of the cervical arteries
24-hour Holter electrocardiography
|
-
Supportive treatment only
-
Corticosteroids are currently not recommended
-
Consider antiplatelet agents in patients with underlying vascular risk factors
-
Intervention directed toward the underlying lesion
|
Aortic dissection
[33] [34] [35]
|
-
Severe, sharp or “tearing” posterior chest or back pain
-
May be associated with an acute neurological deficit
-
Neurological features may include hemiplegia, monoplegia, and paraplegia
|
-
One-third experiences neurological deficits[18]
-
10% of type A dissections may present with only neurological manifestations
-
Weak or absent pulse (15.1%) (carotid, brachial, or femoral)[17]
-
Associated features may include acute myocardial infarction, cardiac tamponade, hemothorax,
hypotension, pain, abdominal pain, back or flank pain, renal failure, or Horner's
syndrome
|
-
ECG to exclude myocardial infarction
-
CXR for mediastinum widening and hemothorax
-
Bedside echocardiogram transesophageal or transthoracic
-
CT aortogram
-
CT head
|
|
Brown–Sequard syndrome
[36] [37]
|
|
-
Ipsilateral weakness
-
Ipsilateral loss of proprioception and vibratory sensation
-
Contralateral loss of pain and temperature sensation
-
Urinary bladder and bowel involvement
|
|
|
Transverse myelitis
[38]
|
-
Isolated spinal cord dysfunction over hours or days
-
Weakness and sensory disturbance below the level of the lesion
-
Back pain with bladder and bowel dysfunction is common
-
No evidence of compressive lesion
-
Segmental spinal cord injury caused by acute inflammation
-
Thoracic cord most commonly involved
-
50% have preceding viral infection
|
-
Evidence of myelopathy, with weakness and sensory symptoms corresponding to a specific
dermatomal and myotomal level
-
Increased or decreased sensation with paresthesia may be present
-
Urinary bladder and bowel involvement
|
MRI is diagnostic
|
-
IV methylprednisolone
-
IVIG
-
Plasma exchange
|
Amyotrophic lateral sclerosis (ALS)
[39] [40] [41] [42]
|
-
Progressive weakness which may start in a limb
-
May manifest by slurred speech and dysphagia
-
A small percentage may have respiratory involvement initially
-
Other neurological symptoms: changes in mental function (e.g., dementia, pseudobulbar
affect
-
Absence of alternative diagnosis
|
-
A mixture of UMN signs and LMN signs
-
The sensory examination is usually normal
-
Spares urinary bladder/ bowel
|
-
Nerve conduction studies
-
Electromyography (EMG)
-
MRI (to exclude other intracranial lesions)
-
To exclude other diagnoses: anti-GM1 antibody (multifocal motor neuropathy), SPEP
(multiple myeloma, lymphoma), heavy metals, HIV, Lyme antibody, myasthenia gravis
-
Lumbar puncture: HIV, Lyme disease or chronic
Inflammatory demyelinating
|
|
Peripheral nerve lesions
|
Guillain–Barré syndrome
[7] [8] [42] [43] [44] [45]
|
-
Precedental history of mild respiratory or gastrointestinal illness (2–4 weeks prior)
-
Typically, symmetrical ascending paralysis with limb paresthesia is common (80%) and pain
-
Dysautonomia occurs in 70%
-
Upper limb/facial weakness (10%)
-
Respiratory failure (~10%)
-
Oculomotor weakness (15%)
|
-
Symmetrical ascending paralysis
-
Absent deep tendon reflexes
-
Miller Fisher syndrome variant presents with ophthalmoplegia, ataxia, and areflexia
-
In acute motor axonal neuropathy variant, sensation is preserved
-
Acute motor and sensory axonal neuropathy has more sensory symptoms
-
Other rarer variants may exist[40]
|
-
CSF analysis: elevated protein, normal cell count
-
Electromyography
-
Nerve conduction studies
-
Glycolipid antibodies may be present in some variants
|
|
Vasculitic neuropathy
[46] [47]
|
-
May be part of systemic vasculitis or a nonsystemic vasculitic neuropathy
-
Asymmetric or multifocal painful sensorimotor neuropathy
-
May present as mononeuritis multiplex or a sensorimotor neuropathy
-
Sensory symptoms of pain, burning, or paresthesias precede and virtually always present
-
Weakness of muscles supplied by the affected nerve
-
Constitutional symptoms, including weight loss, anorexia, fatigue, arthralgia, myalgia,
and fever, occur in approximately two-thirds of patients
|
-
Flaccid asymmetric paresis with sensory abnormalities in variable distributions
-
Lower limbs are more commonly involved
-
Distal involvement is more frequent than proximal
-
Cranial nerve (facial) may be involved in 8% of patients
|
|
|
Toxin-induced peripheral neuropathy
[48] (alcohol, amiodarone, chloramphenicol, disulfiram, isoniazid, lithium, metronidazole,
nitrofurantoin, nitrous oxide, thalidomide, vincristine, thallium, etc.)
|
-
Many drugs and industrial chemicals may cause distal axonopathy
-
Dose, duration of exposure, and host factors affect outcome
-
Presentation with pain, paresthesia, and hypoesthesia in the feet and distal weakness
and gait disturbance
-
Autonomic dysfunction may be present
|
-
Sensory changes in glove and stocking distribution
-
Distal weakness that progresses proximally
-
Hyporeflexia, symmetrical loss of ankle jerks first
-
CNS may be involved
|
|
-
Prevent ongoing exposure
-
Supportive care
|
Heavy metal toxicity
[49] [50] [51]
|
-
Peripheral neuropathies may occur within a few hours to days of acute high dose exposure,
especially lead, arsenic, and thallium[47]
-
Common presentation: nausea, persistent vomiting, diarrhea, and abdominal pain, with
encephalopathy, cardiomyopathy, dysrhythmias, acute kidney injury, and metabolic acidosis
|
-
Lead neuropathy initially affects motor fibers in radial and peroneal distributions
-
Mees lines (horizontal hypopigmented lines across all nails)
-
Evidence of anemia and other major organ failures
|
-
CBC (anemia) with blood film analysis for basophilic stippling (lead/arsenic toxicity),
-
Kidney and liver function tests and coagulation studies
-
Serum and urine metal levels of suspected metal
|
|
Nerve compression syndromes
[52] [53]
(median nerve at wrist, ulnar nerve at elbow and wrist, radial nerve in proximal forearm,
scapular nerve, lateral femoral cutaneous nerve, common peroneal nerve, tibial nerve,
and lower brachial plexus)
|
-
History of acute or prolonged neural pressure
-
History depends on the region involved
-
Pain and paresthesias typically precede hypoesthesia and weakness/atrophy
-
May be caused by systemic conditions such as pregnancy, obesity, hypothyroidism, and
diabetes
-
Local causes such as prolapsed intervertebral disc produces symptoms in the affected
dermatome and myotome
|
-
Weakness in the muscles supplied by the affected nerve
-
Flaccid, hypotonic, hyporeflexic paralysis
-
Sensory symptoms include pain, paresthesias, and hypoesthesia
-
Wasting and atrophy if long standing
-
Skin changes include dry, thin, hairless skin; ridged, thickened, cracked nails; and
recurrent skin ulceration
|
-
Nerve conduction studies
-
MRI
-
EMG
|
|
Neuromuscular junction
|
Botulism
[53] [54] [55] [56]
|
-
Descending symmetrical paralysis with a clear sensorium and no fever
-
No sensory deficits other than blurred vision
-
Foodborne
Seen after 12–36 hours of ingestion
Prodromal symptoms including nausea, vomiting, abdominal pain, diarrhea, and dry mouth
with sore throat[42]
-
Wound botulism
Follow deep infected regions with the presence of spores
-
Infantile botulism
Occurs from 1 week–1 year in infants who are formula fed
-
May present with constipation, weakness, feeding difficulties, descending or global
hypotonia, drooling, anorexia, irritability, and weak cry[43]
|
-
Cranial nerves first affected: fixed dilated pupils (causing blurred vision), diplopia,
nystagmus, ptosis, dysphagia, dysarthria, and facial weakness
-
Descending flaccid paralysis
-
May cause bladder and bowel dysfunction
|
-
Stool, vomit, suspected food and wound debridement looking for C. botulinum spores
-
Serum assay for botulinum toxin
-
Pulmonary function tests
|
-
Adults/Children > 1 year: Equine serum heptavalent
-
Infants < 1 year: Human-derived botulism immune globulin
-
Penicillin G (or metronidazole) for wound
|
Tick paralysis
[57] [58]
|
-
Presents with unsteady gait followed by an ascending symmetrical flaccid paralysis
2–6 days post tick attachment
-
Sensory symptoms: paresthesias and hypoesthesia
-
Anorexia, lethargy, drowsiness, and confusion may precede weakness
-
Ataxia may be only symptom
-
No fever
|
-
Tick found attached to patient
-
Ascending symmetrical flaccid paralysis
-
Hypotonic, hyporeflexic
-
Progresses to affect all cranial nerves including pupillary dilatation
-
Sensory function is generally preserved other than mild paresthesias and hypoesthesia
|
-
Locate tick
-
EMG shows reduced amplitude of compound muscle action potentials
-
Labs, CSF analysis, and MRI are typically normal
|
|
Organophosphate toxicity
[59] [60]
|
-
Insecticide exposure (e.g., malathion, parathion, diazinon, fenthion, dichlorvos,
chlorpyrifos, ethion)
-
Nerve gas exposure (e.g., sarin, VX, soman, tabun)
-
Ophthalmic agents (e.g., echothiophate, isoflurophate)
-
Antihelminthics (trichlorfon)
|
-
Fasciculations with paralysis
-
Cholinergic symptoms: Bronchospasm, bradycardia, miosis, lacrimation, salivation,
bronchorrhea, urination, emesis, and diarrhea
-
Decreased deep tendon reflexes,
-
cranial nerve abnormalities including bulbar palsy
-
Respiratory insufficiency
-
Delayed ascending flaccid paralysis may develop
|
|
-
Remove contaminated clothes
-
Care of airway, breathing, and circulation
-
Atropine 2–3 mg IV stat, then double the dose every five minutes until symptoms are
controlled
-
Pralidoxime
-
Consider benzodiazepines for the prevention and treatment of seizures
|
Myasthenia gravis
[61] [62]
|
-
History of myasthenia gravis
-
Acute decompensation (myasthenic crisis) may be spontaneous or precipitated by infection,
surgery, or tapering of immunosuppression, certain antibiotics and other precipitating
factors
-
Excessive treatment with cholinesterase inhibitors may paradoxically cause weakness
(Cholinergic crisis)
|
-
85% of patients have involvement of the eyelids and extra-ocular muscles, resulting
in ptosis and/or diplopia[23]
-
Fatiguability
-
Flaccid muscles weakness
-
Central muscles are predominantly involved such as bulbar muscles
-
Neck and proximal limb weakness may occur
-
Respiratory failure occurs in 1%
-
Weakness increases after exertion
|
-
Ice pack test (e.g., ice on affected eyelid improves ptosis)
-
ACh receptor antibodies if diagnosis uncertain
-
Pulmonary function tests
-
Consider arterial blood gas
-
Consider CT chest (thymoma may affect breathing)
|
-
For acute decompensation, admit to ICU
-
Airway and ventilation should be assessed and managed with either non-invasive ventilation
or intubation
-
Withdraw anticholinesterase medications
-
Plasmapheresis or IVIG
-
High-dose steroids
-
Consider other immunosuppressants
|
Lambert–Eaton myasthenic syndrome (LEMS)
[63] [64]
|
-
In 40% of patients, small cell lung cancer is present
-
Progressive proximal lower limb weakness
-
Ptosis, diplopia, and dysarthria as cranial nerves become involved, (less common than
myasthenia gravis)
-
Autonomic dysfunction
-
Exacerbated by heat or fever and certain drugs
|
-
Proximal muscle weakness, lower limbs more than upper
-
Depressed tendon reflexes
-
Post-tetanic potentiation
-
Sensation preserved
-
Respiratory failure rare
|
-
Voltage gated calcium channel antibodies
-
AChR antibodies
-
Repetitive nerve stimulation
-
EMG
-
Look for malignancy with imaging/Bronchoscopy
|
-
Confirm diagnosis and distinguish from myasthenia gravis before starting treatment
-
Supportive treatment
-
Treat underlying malignancy
-
Consider 3,4-diaminopyridine
-
IVIG
-
Plasma exchange
|
Muscle
|
Dermatomyositis
[65]
|
-
May present with skin and/or muscle involvement
-
Proximal muscle weakness
-
Characteristic rash
-
Systemic symptoms include arthralgia, arthritis, dyspnea, dysphagia, arrhythmia, and
dysphonia
|
-
Heliotrope rash (blue-purple discoloration on the upper eyelids)
-
Raised, violaceous, scaly eruption on the knuckles (Gottron’s papules)
-
Proximal symmetrical muscle weakness
-
Muscle pain and tenderness
-
Normal sensation and tendon reflexes
-
Joint swelling (particularly of the hand) may occur occasionally in some patients
|
|
|
Generalized weakness due to systemic causes
|
Hyperglycemia
[66] [67]
|
-
History of diabetes
-
Possible precipitating events (e.g., infection, myocardial infarction, surgery, critical
illness)
-
Neurological symptoms primarily occur when plasma osmolality is greater than 320 mOsmol/L
-
Neurological symptoms may include hemiparesis, focal motor deficits, decreased consciousness,
and seizures
-
May have polyuria, polydipsia, and weight loss for several days before presentation
|
-
Level of consciousness may be reduced
-
Focal motor and sensory deficits including aphasia, hyperreflexia, hemianopia, and
brainstem dysfunction
-
Other findings associated with DKA or HHS include evidence of volume depletion, hyperventilation
and abdominal pain
|
-
Serum glucose
-
Plasma osmolality
-
Serum electrolytes (with anion gap), urea, and creatinine
-
Urinalysis, and urine/ serum ketones by dipstick
-
Blood gas
-
Electrocardiogram
-
CT head to exclude other causes
|
-
Fluid replacement to correct hypervolemia and hyperosmolality
-
Insulin infusion
-
Close monitoring of urine output and electrolytes (potassium, magnesium, and phosphate)
-
Treat precipitating cause
|
Hypoglycemia (serum glucose<3 mmol/L; <50 mg/dL)
[68]
|
-
Diabetes
-
Insulin regimen
-
Oral hypoglycemics
-
Alcohol
-
Sepsis
-
Liver disease
-
Hypocortisolemia
|
-
Decreased consciousness
-
Many forms of focal neurological deficit possible, which may mimic
-
Dysphoria
-
Seizures stroke
-
Tremor, palpitations, anxiety, sweating, hunger, and paresthesia
|
|
|
Hyponatremia, hypernatremia
[69] [70]
|
-
Hyponatremia: diuretic overdose, hypervolemia, CHF, cirrhosis, SIADH, cerebral salt wasting and
water intoxication
-
Hypernatremia: dehydration, pituitary insufficiency, iatrogenic sodium supplementation
-
Lethargy and confusion are most common followed by seizures and coma in both extremes
|
|
|
-
Hyponatremia: fluid restriction, stop diuretics, avoid rapid correction
-
Hypernatremia: IV fluids if hypovolemic, prefer hypotonic solutions (5D, 0.45% NS), avoid rapid
correction
-
if urine specific gravity is low (pituitary insufficiency): administer desmopressin
|
Hypermagnesemia
[71]
|
-
Typically follows excessive magnesium administration (e.g., management of pre-eclampsia)
in context of renal impairment
-
Lethargy and confusion are most common neurologic manifestations followed by generalized
weakness, and respiratory failure
|
|
Serum magnesium levels
|
|
Hypophosphatemia
[72] [73]
|
-
Causes of hypophosphatemia include:
-
Intracellular shift: refeeding syndrome, respiratory alkalosis, diabetic ketoacidosis, rapidly growing
malignancies, osmotic diuresis, malabsorption, renal tubular acidosis
-
Increased urinary excretion: primary or secondary hyperparathyroidism, osmotic diuresis, renal tubular acidosis,
transplanted kidneys, Fanconi syndrome, etc.
-
Decreased intestinal absorption: diarrhea, malabsorption syndromes,
-
phosphate binders
-
Decreased dietary intake: anorexia nervosa or chronic alcoholism, Hypothermia
-
Painful proximal myopathy
-
Other symptoms: changes in mental function, seizures, neuropathies, arrhythmias, skeletal
muscle weakness, respiratory failure, rhabdomyolysis, leucocyte dysfunction, sepsis,
and sudden death
|
-
Proximal muscle weakness is common
-
Any muscle group may be involved in various combinations, ranging from ophthalmoplegia
to proximal myopathy to dysphagia or ileus
-
Weakness may be so profound as to mimic Guillain–Barre syndrome
-
Neurological features: Confusion, seizures, and coma
-
Cardiac contractility may be impaired leading to global myocardial depression
|
|
|
Periodic paralysis (PP)
[74]
|
-
Repeated episodes of flaccid muscle weakness occurring at irregular intervals with
normal strength between episodes
-
Usually hereditary
-
Various types of periodic paralysis exist, including:
-
Hyperkalemic PP
-
Hypokalemic PP
-
Paramyotonia congenita
-
Thyrotoxic PP
-
Andersen-Tawil syndrome
-
Look for precipitating factor (e.g., post exercise, fasting, cold alcohol, stress,
and duration of episode)
|
|
-
Serum potassium
-
Elevated creatine kinase (CK)
-
Potassium: creatinine ratio
-
Blood gas analysis for evidence of concomitant metabolic acidosis or alkalosis
-
ECG
-
EMG
-
Nerve conduction studies
|
-
Hyperkalemic PP:
-
Hypokalemic PP:
-
Thyrotoxic PP:
-
Beta blockers
-
Treat thyrotoxicosis
-
Andersen–Tawil syndrome:
-
Acetazolamide
|
Miscellaneous
|
Envenomation
[75] [76]
|
-
Snake bite
[16]
-
Scorpion sting
-
Marine envenomation
-
Ingestion of puffer fish
|
-
Snake bites[16]:
Cardiovascular: hypotension, shock, arrest
-
Neurological: paralysisptosis, diplopia, bulbar palsy, dysarthria; respiratory muscle
paralysis
Coagulopathy: intracranial hemorrhage, bleeding from bite site, ecchymoses, bleeding
gums, hemarthroses
Rhabdomyolysis: tender muscles
-
Scorpion sting: cranial nerve and somatic skeletal neuromuscular dysfunction, with
pain and paresthesia
-
Blue-ringed octopus and puffer fish envenomation: descending symmetrical flaccid paralysis
with clear sensorium, nausea, and vomiting, blurred vision, ataxia, respiratory failure
-
Stonefish envenomation: weakness in the affected limb, severe pain, shock
|
-
Serial bedside pulmonary function tests if descending paralysis
-
Other investigations as CBC, LFTs, CK, whole blood clotting time, coagulation, screen,
D-dimer, fibrinogen levels, urinalysis for blood (myoglobin),
-
Head-CT if decreased GCS
-
Use venom detection kit for bite swab and urine
|
-
Supportive care of airway, breathing, and circulation
-
Pressure immobilization bandage
-
Specific antivenom
|
Locked-in syndrome
[77]
|
-
Sudden onset tetraplegia, facial weakness, and horizontal gaze palsy
-
Causes ischemic stroke (most common), central pontine myelinolysis, encephalitis,
or tumor
|
-
Flaccid symmetrical tetraparesis
-
Consciousness preserved or may be affected initially but returns to normal
-
Voluntary vertical eye and eyelid movements preserved
-
Hearing, vision, pupillary reflexes, and sensation all normal
|
|
Follow acute stroke protocol
|
Acute porphyria
[78]
|
-
Abdominal pain: may begin in chest or back and move to abdomen
-
Gastrointestinal symptoms such as vomiting, diarrhea, and constipation are common
-
Psychiatric symptoms
-
Acute weakness (early or late)
-
May develop seizures
-
Certain medications are known to exacerbate
|
-
Muscle weakness usually begins proximally and more often in upper limbs
-
Symmetrical hypotonia
-
Hyporeflexic
-
Flaccid paralysis
-
No rash unlike other forms of porphyria
-
Tachycardia and hypertension may be present
|
|
|
Diabetic lumbosacral radiculoplexus neuropathy
[79]
|
-
Diabetes mellitus with proximal weakness
-
Asymmetrical pain in the hip, buttock, or thigh
-
Associated with poor glycemic control
-
Patients without distal symmetrical polyneuropathy most often have sudden, unilateral
onset
-
Occasionally may be initial presentation of diabetes mellitus
|
-
Proximal lower limb muscle weakness and wasting
-
Minimal sensory loss is observed
-
Knee-jerk reflex is absent, with commonly preserved ankle jerks
-
Ankle jerks may also be absent, with underlying distal symmetrical polyneuropathy
|
|
|
Psychiatric illness
|
-
No history suggestive of any physical illness
-
Temporal associations with psychosocial stressors
-
Symptom substitution frequently present
-
Primary psychological or personal gain present
|
-
La belle indifference present
-
Distribution does not follow anatomical pattern
-
Presence of affective or emotional disturbances on mental status examination
|
-
Relevant investigations to rule out organic lesions like (MRI/CT, EEG).
-
Visual-evoked potentials and brainstem auditory evoked responses to rule out malingering/compensation
neurosis
|
|