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Focal neurologic signs

From Wikipedia, the free encyclopedia

Focal neurologic signs
Differential diagnosisHead trauma, Tumor, Stroke

Focal neurologic signs also known as focal neurological deficits or focal CNS signs are impairments of nerve, spinal cord, or brain function that affects a specific region of the body, e.g. weakness in the left arm, the right leg, paresis, or plegia.[citation needed]

Focal neurological deficits may be caused by a variety of medical conditions such as head trauma,[1] tumors or stroke; or by various diseases such as meningitis or encephalitis or as a side effect of certain medications such as those used in anesthesia.[2]

Neurological soft signs, are a group of non-focal neurologic signs.[3]

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Transcription

Frontal lobe signs

Frontal lobe signs usually involve the motor system and may include many special types of deficit, depending on which part of the frontal lobe is affected:[citation needed]

  • unsteady gait (unsteadiness in walking)
  • muscular rigidity, resistance to passive movements of the limbs (hypertonia)
  • paralysis of a limb (monoparesis) or a larger area on one side of the body (hemiparesis)
  • paralysis head and eye movements
  • inability to express oneself linguistically, described as an expressive aphasia (Broca's aphasia)
  • focal seizures that may spread to adjacent areas (Jacksonian seizure)
  • grand mal or tonic-clonic seizures
  • changes in personality such as disinhibition, inappropriate jocularity, rage without provocation; or loss of initiative and concern, apathy, akinetic mutism, general retardation
  • "frontal release" signs, i.e. reappearance of primitive reflexes such as the snout reflex, the grasp reflex, and the palmar-mental reflex
  • unilateral loss of smell (anosmia)

Parietal lobe signs

Parietal lobe signs usually involve somatic sensation, and may include:[citation needed]

  • impairment of tactile sensation
  • impairment of proprioception, i.e. postural sensation and sensation of passive movement
  • sensory and visual neglect syndromes, i.e. inability to pay attention to things in certain parts of the person's sensory or spatial environment; this may be as extreme as denial of a limb
  • loss of ability to read, write, or calculate (dyslexia, dysgraphia, dyscalculia)
  • loss of ability to find a defined place (geographical agnosia)
  • loss of ability to identify objects based on touch (astereognosia)

Temporal lobe signs

Temporal lobe signs usually involve auditory sensation and memory, and may include:[citation needed]

Occipital lobe signs

Occipital lobe signs usually involve visual sensation, and may include:[citation needed]

  • total loss of vision (cortical blindness)
  • loss of vision with denial of the loss (Anton's syndrome)
  • loss of vision on one side of the visual field of both eyes (homonymous hemianopsia)
  • visual agnosias, i.e. inability to recognize familiar objects, colors, or faces
  • visual illusions such as micropsia (objects appear smaller) and macropsia (objects appear larger)
  • visual hallucinations, displaying elementary forms, such as zig-zags and flashes, in one half of the visual field only for each eye (in contrast, temporal lobe visual hallucinations display complex forms, and fill the entire visual field)

Limbic signs

Damage to the limbic system involves loss or damage to memory, and may include:[citation needed]

  • loss or confusion of long-term memory prior to focal neuropathy (retrograde amnesia)
  • inability to form new memories (anterograde amnesia)
  • loss of, or reduced emotions (apathy)
  • loss of olfactory functions
  • loss of decision-making ability

Cerebellar signs

Cerebellar signs usually involve balance and coordination, and may include:[citation needed]

  • cerebellar ataxia a gait with a broad base; the patient falters to the side of the lesion (ataxia)
  • inability to coordinate fine motor activities (intention tremor), e.g. "past-pointing" (pointing beyond the finger in the finger-nose test)
  • inability to perform rapid alternating movements (dysdiadochokinesia), e.g. inability to rapidly flip the hands
  • involuntary horizontal eye movements (nystagmus)
  • dysarthria, usually with bilateral lesions; the speech has a halting jerking quality (scanning speech or staccato speech)

Brainstem signs

Brainstem signs can involve a host of specific sensory and motor abnormalities, depending on which fiber tracts and cranial nerve nuclei are affected.[citation needed]

Spinal cord signs

Spinal cord signs generally involve unilateral paralysis with contralateral loss of pain sensation.[citation needed]

Neurological soft signs

Neurological soft signs (NSS) are a group of minor non-focal neurological signs that include synkinesis.[3] Other soft signs including clumsiness, and loss of fine motor movement are also commonly found in schizophrenia.[4] NSS likely reflect impairments in sensory integration, motor coordination, and the carrying out of complex motor tasks.[3] When associated with schizophrenia the signs stop if clinical symptoms are effectively treated; and a consensus suggests that they may constitute a state marker for schizophrenia.[3]

See also

References

  1. ^ Thiruppathy, S. P.; Muthukumar, N. (2004). "Mild head injury: Revisited". Acta Neurochirurgica. 146 (10): 1075–82, discussion 1082-3. doi:10.1007/s00701-004-0335-z. PMID 15744844. S2CID 13150034.
  2. ^ Thal, G. D.; Szabo, M. D.; Lopez-Bresnahan, M.; Crosby, G. (1996). "Exacerbation or unmasking of focal neurologic deficits by sedatives". Anesthesiology. 85 (1): 21–5, discussion 29A-30A. doi:10.1097/00000542-199607000-00004. PMID 8694368. S2CID 8984607.
  3. ^ a b c d Fountoulakis, KN; Panagiotidis, P; Kimiskidis, V; Nimatoudis, I; Gonda, X (February 2019). "Neurological soft signs in familial and sporadic schizophrenia". Psychiatry Research. 272: 222–229. doi:10.1016/j.psychres.2018.12.105. PMID 30590276. S2CID 56476015.
  4. ^ Ferri, Fred F. (2019). Ferri's clinical advisor 2019 : 5 books in 1. pp. 1225–1226. ISBN 9780323530422.

Essentials of Kumar and Clark's Clinical Medicine, 5th Edition. Saunders Elsevier, UK. 2012. page 725

This page was last edited on 12 August 2023, at 18:43
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