Night genetic, it cannot (Aranda, 2014; Leroy, 2011).

Night blindness, also referred to as
nyctalopia, is a condition in which an individual is unable to see in faint
light or the dark as a result of “inadequate synthesis of rhodopsin . . .

vitamin A deficiency, retinal degeneration, or a congenital defect” (Colman, 2015).

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Night blindness is generally a symptom of another condition which affects a
professionals ability to rectify the condition as it is dependent on the method
in which it was acquired; if it was obtained as a symptom, it can be treated
but if it is genetic, it cannot (Aranda, 2014; Leroy, 2011). The types of night
blindness not attributed to genetics most discussed in research are night
blindness as a symptom of iostretinoin and as a symptom of Crohn’s disease.

Night blindness acquired as a result of genetics is X-linked congenital
stationary night blindness (X-linked CSNB).

Isotretinoin is used as a treatment
for acne where four to six percent of patients utilizing this medication have
developed night blindness (Teo & Yazdabadi, 2013). Isotretinoin use
may result in night blindness as it inhibits the 11-cisretinol dehydrogenase
which slows the synthesis of 11-cisretinaldehyde and the regeneration of
rhodopsin (Teo & Yazdabadi, 2013).  This results in the inability to see in dim
light or the dark as the rods do not adapt to the dark (Teo & Yazdabadi,
2013). In order to treat night blindness as a symptom of isotretinoin it is recommended
to stop utilizing the medication and consume vitamin A supplements as
11-cisretinaldehyde is derived from vitamin A (Teo & Yazdabadi, 2013).

Crohn’s disease
is an inflammation of the gastrointestinal tract (da Rocha Lima, Pichi, &
Lowder, 2014). Individuals with Crohn’s disease frequently undergo a procedure
which removes a damaged part of the gastrointestinal tract which puts them at
risk of malnutrition and especially vitamin A deficiency (da Rocha Lima, Pichi,
& Lowder, 2014). As a result of vitamin A deficicency, rod function is
depleted and cone amplitudes are reduced which is indicative of


lack of repolarization as well as
possible retinal degeneration (da Rocha Lima, Pichi, & Lowder, 2014; Wu
& Fawzi, 2012). The ability of the cones and rods to adjust to the dark is
severely limited (da Rocha Lima, Pichi, & Lowder, 2014). This condition can
be treated with a course of vitamin A supplements as vitamin A, also referred
to as retinol, plays a significant role in converting nerve impulses into
images in the retina (da Rocha Lima, Pichi, & Lowder, 2014; Selner, 2016).

X-linked CSNB is present from birth and is split into
two types: complete and incomplete (Dinet et al., 2016). Complete X-linked CSNB
is characterized by an absent b-wave which means that the photoreceptors are
unable to send signals to the bipolar cells which in turn means that ganglion
cells are unable to receive that signal and send the information to the rest of
the brain (Boycott, Sauve, & MacDonald, 2008; Dinet et al., 2016).

Incomplete X-linked CSNB is characterized by reduced b-waves and cone function
(Boycott, Sauve, & MacDonald, 2008). 
Both forms of X-linked CSNB are caused by a mutated gene and are
characterized by a reduced or absent b-wave after a bright flash following dark
adaptation (Boycott, Sauve, & MacDonald, 2008). There is currently no
treatment to correct this condition.